The most common food additives and ingredients.
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Barely three months into the new year and we are happy to announce a monumental milestone reached - 150 million downloads.
\n\nThis achievement solidifies IntechOpen’s place as a pioneer in Open Access publishing and the home to some of the most relevant scientific research available through Open Access.
\n\nWe are so proud to have worked with so many bright minds throughout the years who have helped us spread knowledge through the power of Open Access and we look forward to continuing to support some of the greatest thinkers of our day.
\n\nThank you for making IntechOpen your place of learning, sharing, and discovery, and here’s to 150 million more!
\n\n\n\n\n'}],latestNews:[{slug:"intechopen-signs-new-contract-with-cepiec-china-for-distribution-of-open-access-books-20210319",title:"IntechOpen Signs New Contract with CEPIEC, China for Distribution of Open Access Books"},{slug:"150-million-downloads-and-counting-20210316",title:"150 Million Downloads and Counting"},{slug:"intechopen-secures-indefinite-content-preservation-with-clockss-20210309",title:"IntechOpen Secures Indefinite Content Preservation with CLOCKSS"},{slug:"intechopen-expands-to-all-global-amazon-channels-with-full-catalog-of-books-20210308",title:"IntechOpen Expands to All Global Amazon Channels with Full Catalog of Books"},{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"}]},book:{item:{type:"book",id:"59",leadTitle:null,fullTitle:"Recent Hurricane Research - Climate, Dynamics, and Societal Impacts",title:"Recent Hurricane Research",subtitle:"Climate, Dynamics, and Societal Impacts",reviewType:"peer-reviewed",abstract:"This book represents recent research on tropical cyclones and their impact, and a wide range of topics are covered. An updated global climatology is presented, including the global occurrence of tropical cyclones and the terrestrial factors that may contribute to the variability and long-term trends in their occurrence. Research also examines long term trends in tropical cyclone occurrences and intensity as related to solar activity, while other research discusses the impact climate change may have on these storms. The dynamics and structure of tropical cyclones are studied, with traditional diagnostics employed to examine these as well as more modern approaches in examining their thermodynamics. \n\nThe book aptly demonstrates how new research into short-range forecasting of tropical cyclone tracks and intensities using satellite information has led to significant improvements. In looking at societal and ecological risks, and damage assessment, authors investigate the use of technology for anticipating, and later evaluating, the amount of damage that is done to human society, watersheds, and forests by land-falling storms. The economic and ecological vulnerability of coastal regions are also studied and are supported by case studies which examine the potential hazards related to the evacuation of populated areas, including medical facilities. These studies provide decision makers with a potential basis for developing improved evacuation techniques.",isbn:null,printIsbn:"978-953-307-238-8",pdfIsbn:"978-953-51-4907-1",doi:"10.5772/592",price:159,priceEur:175,priceUsd:205,slug:"recent-hurricane-research-climate-dynamics-and-societal-impacts",numberOfPages:632,isOpenForSubmission:!1,isInWos:1,hash:"603bbf36aa423b62f05802dabb4a4b6b",bookSignature:"Anthony Lupo",publishedDate:"April 19th 2011",coverURL:"https://cdn.intechopen.com/books/images_new/59.jpg",numberOfDownloads:74478,numberOfWosCitations:59,numberOfCrossrefCitations:32,numberOfDimensionsCitations:71,hasAltmetrics:0,numberOfTotalCitations:162,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"May 11th 2010",dateEndSecondStepPublish:"June 8th 2010",dateEndThirdStepPublish:"October 13th 2010",dateEndFourthStepPublish:"November 12th 2010",dateEndFifthStepPublish:"January 11th 2011",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,7",editedByType:"Edited by",kuFlag:!1,editors:[{id:"18289",title:"Prof.",name:"Anthony",middleName:"Rocco",surname:"Lupo",slug:"anthony-lupo",fullName:"Anthony Lupo",profilePictureURL:"https://mts.intechopen.com/storage/users/18289/images/system/18289.png",biography:"Dr. Anthony R. Lupo is an Atmospheric Sciences Professor in the School of Natural Resources at the University of Missouri. He earned his BSc degree from the State University of New York at Oswego in 1988, and his M.S. and Ph.D. degrees from Purdue University in 1991 and 1995. His research is in large-scale atmospheric dynamics, climate dynamics, and climate change, and he has more than 130 peer-reviewed publications. Additionally, he edited the books; Recent Hurricane Research: Climate, Dynamics, and Societal Impacts (2011), and Recent Developments in Tropical Cyclone Dynamics, Prediction, and Detection (2016) with IntechOpen. He is a member of the American Meteorological Society, National Weather Association, Royal Meteorological Society (Fellow), American Geophysical Union, Sigma Xi, Gamma Sigma Delta, Phi Kappa Phi, and Missouri Academy of Science (Fellow). He was a Fulbright Scholar to Russia (summer 2004) at the Russian Academy of Sciences in Moscow. 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The history of food additives goes back to ancient times. As great civilisations developed, populations grew and so did the demand for food. In ancient Egypt, where the climate was not conducive to food storage, especially due to the heat, people started looking for ways to extend the usability life of products. Common practices included the addition of salt, drying in the sun, curing/corning, meat and fish smoking, pickling, and burning sulphur during vegetable preservation. The earliest preservatives included sulphur dioxide (E220), acetic acid (E260), and sodium nitrite (E250), while turmeric (E100) and carmine (E120) were among the first colours. Food preservation was also of immense importance during numerous armed conflicts. Both during the Napoleonic wars in Europe and during the American Civil War, seafarers and soldiers needed food. Limited access to fresh food at the front motivated the armed forces to transport their food with them. This is when cans were introduced for food preservation purposes. In the subsequent centuries, ammonium bicarbonate (E503ii), also known as salt of hartshorn, used as a rising agent for baked goods, and sodium hydroxide solution (E524), used in the production of salty sticks, rose to prominence [1, 2].
\nThe nineteenth century saw considerable advancements in the fields of chemistry, biology, and medicine. A name that needs to be mentioned here is Louis Pasteur, a French scientist, who studied microbiology, among other things. He was the first to prove that microorganisms were responsible for food spoilage. At the same time, new chemical compounds were discovered that were able to inhibit the growth of microbes. Some substances, such as picric acid, hydrofluoric acid, and their salts, often had disastrous consequences when added to food. Insufficient knowledge of toxicology resulted in consumer poisonings and even deaths [1, 3]. At that time, food preservation was the number one priority, which was achieved, for instance, by using salicylic acid, formic acid (E236), benzoic acid (E210), boric acid (E284), propionic acid (E280), sorbic acid (E200) and its potassium salt (E202), and esters of p-hydroxybenzoic acid. Later, food concerns also focused on improving the organoleptic properties of their products and started to enhance food with colours, flavours, and sweeteners, without first researching their effects on human health. For example, such practices involved the use of synthetic colours used in fabric dyeing. This desire to make money on beautiful-looking products led to adulterating food with copper and iron salts, which have a negative impact on the human body. It was as late as in 1907 that the United States studied 90 of the synthetic colours used at that time for food dyeing and found only 7 to be acceptable for further use. Detailed studies and strict regulations on the use of food additives were created almost a century later [1, 4].
\nGlobally, food safety is ensured by the World Health Organization (WHO) and the Food and Agriculture Organization (FAO). In 1962, these organisations established a special agenda—the Codex Alimentarius Commission. The Commission has prepared and updated the Codex Alimentarius, which is not a legal Act per se, but provides a reference for standards on raw materials and food products, acceptable contamination levels, hygienic processing, research methods, and food additives for almost all countries worldwide [5]. In the European Union, the body responsible for improving human health protection and food safety risk mitigation, as well as for taking care of purchaser interests, is the European Food Safety Authority (EFSA). It is a scientific agency established in 2002 pursuant to the Regulation of the European Parliament and of the Council of 28 January 2002. European legislation is based on the Codex Alimentarius but conducts its own complementary research. Therefore, the list of food additives permitted by the European Union is different from the American one [5].
\nThe primary legal Act governing food in Poland is the Food and Nutrition Safety Act of 25 August 2006 (as amended). It specifies the requirements applicable to food and nutrition, concerning product labelling, hygienic conditions throughout the production process, and product replacement rules, as well as requirements concerning the use of food additives. The key document that pertains specifically to food additives is the Regulation of the European Parliament and of the Council of 16 December 2008 on food additives. The EU-approved list of food additives is presented in the Commission Regulation (EU) of 11 November 2011 [4, 5].
\nA
EU legislation has approved approximately 330 food additives for use. The primary objectives behind the use of additives are to extend the shelf life and freshness of products, prevent product quality impairment, make the product more attractive to customers, achieve the desired texture, ensure specific product functionality, facilitate production processes, reduce production costs, and enrich the nutritional value of products. In order to harmonise, effectively identify any additives, and ensure smooth exchange of goods, each food additive has its own, standardised, code. This code is consistent with the International Numbering System (INS) and comprises the letter “E” and three or four digits. There are several food additive classifications. One is based on the regulation and differentiates between colours (approx. 40), sweeteners (approx. 16), and other additives (approx. 277) [8, 9].
\nColours—E100–E199
Preservatives and acidity regulators—E200–E299
Antioxidants and synergists—E300–E399
Stabilising, thickening, emulsifying, coating, and bulking substances—E400–E499
Other substances—E500 and above
Food additives can also be divided into four major groups, based on their processing purpose. These are substances that prevent food spoilage, those which improve sensory features, firming additives and excipients. The most numerous group among additives that slow down food spoilage are
Other substances used as preservatives are
Not only microorganisms but also oxygen is responsible for food spoilage. Products such as oils, fats, and dry goods (flour, semolina) oxidise when they come into contact with atmospheric oxygen. Fat oxidisation (rancidification) occurs in oils, lard, flour, and milk powder. The browning of fruit, vegetables, and meat, on the other hand, is the result of non-fat substance oxidisation. These oxidisation processes can be slowed down or eliminated completely using
In order to extend the freshness of consumer goods, products are also packaged in a modified atmosphere. As part of this process, the oxygen content inside the packaging is reduced and replaced with other
The organoleptic properties of consumer goods are very important to consumers. Visual appeal is considered to be as important as taste or smell. This is where
Synthetic food colours are very competitive compared to natural ones. They offer a wide spectrum of colours, including those that are not available in nature, provide strong colouring, and are resistant to environmental factors, so they do not fade during processing. Furthermore, they are not expensive to produce, which contributes to low end-product prices. Synthetic colours can be divided into organic and inorganic, with organic constituting the considerable majority in terms of food colouring. In the past, chemical colours were made of coal, while now crude oil is used for this purpose. EU law approves 15 synthetic colours, including the so-called Southampton colours. A study conducted in 2007 in the United Kingdom (in Southampton, hence the name) showed the particularly negative effects of six colours on children’s health [10]. Specifically, tartrazine (E102), quinoline yellow (E104), sunset yellow (E110), azorubine (E122), cochineal red (E124), and Allura red AC (E129) were found to cause hyperactivity. As a result, since 2010, manufacturers which add at least one of their products have been required to provide label information about their negative effects on concentration and brain functioning in children. Acceptable daily doses of these colours have also been reassessed and updated. Moreover, research conducted on lab animals has shown that the long-term use of synthetic colours, and especially the three that account for 90% of the use of all synthetic colours (Allura red, tartrazine, and sunset yellow), can cause cancer, allergies, and chromosome mutations. Products that are most often synthetically coloured include candy, wine gums, ready-made desserts, and refreshing beverages [8, 10].
\nDuring consumption, one can experience product taste, smell, and consistency. These three sensations are referred to as palatability and are caused by
A separate group that enhances the sensory properties of food are
The additives that are vital in terms of processing are
What is also important in creating product structure are
Nowadays, consumer goods are widely available, and consumers are provided with a broad range of products to choose from. The continuously growing number of world population (approximately 7 billion in 2011) has made supply on the food market exceed demand. This situation is characteristic of countries with a high GDP. Food producers examine consumer behaviour patterns to see what encourages them to make a purchase, and also the purchase itself and its consequences, and then analyse these processes to launch a new product or a substitute for an already existing one. To sum up, the market has provided more food products than consumers are able to purchase, which results in unimaginable food wastage. Each year, approximately 100 million tonnes of food goes to waste in Europe. This quantity does not include agricultural and food waste or fish discards [13].
\nThe methodology of this study was based on the information contained on the labels. The chemical composition of the investigated food products was presented. Interview with the store’s seller concerned the popularity and frequency of sales listed in the product tables. It should be noted that the examined store is representative when it comes to this type of stores in the majority of small towns in south-eastern Poland.
\nThis study was based on data on the most frequently chosen consumer goods in a store in a small town in Poland. The town is located in a commune that has 5300 residents. Data were obtained by monitoring the sales over the course of 12 months. These products are presented in Tables 2, 3, 4, 5, 6 and classified into the following categories: (i) meat and fish; (ii) beverages; (iii) condiments; (iv) ready-made sauces, soups, and dishes; and (v) sweets and desserts. The main classification criterion was segregation into primary food groups. The chemical composition of each product, as listed on the packaging, was included in a table and then assessed against the presence of any food additives. Sixteen most common additives were selected in all the investigated products; only chemical compounds that were found in at least four food products were taken into consideration. The most common food additives were highlighted in Holt in the “product composition” column and presented in Table 1, together with their E codes. Then, based on the literature, the study described the most common additional substances.
\nName | \nSymbol | \nNumber of products | \n
---|---|---|
Citric acid | \nE330 | \n15 | \n
Monosodium glutamate | \nE621 | \n10 | \n
Guar gum | \nE412 | \n8 | \n
Sodium nitrite | \nE250 | \n7 | \n
Disodium 5′-ribonucleotides | \nE635 | \n6 | \n
Sodium erythorbate | \nE316 | \n5 | \n
Glucose-fructose syrup | \nNot considered an additive | \n5 | \n
Soy lecithin | \nNot considered an additive | \n5 | \n
Maltodextrin | \nNot considered an additive | \n5 | \n
Triphosphates | \nE451 | \n4 | \n
Xanthan gum | \nE415 | \n4 | \n
Carrageenan | \nE407 | \n4 | \n
Tocopherols | \nE306 | \n4 | \n
Glucose syrup | \nNot considered an additive | \n4 | \n
Sodium benzoate | \nE211 | \n4 | \n
Ammonia caramel | \nE150c | \n4 | \n
The most common food additives and ingredients.
Table 1 shows 16 of the most popular substances found in food. The majority of these substances are food additives; four other substances are not considered in the European Union as food additives. The additives that are the most frequently found in the food products examined in this study are citric acid (E330), monosodium glutamate (E621), and guar gum (E412). In Ref. [16] it is reported that the most popular preservatives found in food are the mixture of sodium benzoate and potassium sorbate, or potassium sorbate (E202) and sodium benzoate (E211) used separately, and also ulphur dioxide (E220). Data presented in Table 1 shows that, compared to citric acid, another preservative, sodium benzoate, is used rarer. No potassium sorbate was found in any of the products examined in this study. In Ref. [13] it can be concluded that the most commonly used preservatives and antioxidants are sorbic acid and its salts (E200-203), benzoic acid and its salts (E210-213), sulfur dioxide (E220), sodium nitrite (E250), lactic acid (E270), citric acid (E330) and tocopherols (E306). The majority of the additives listed in Ref. [13] can be found in Table 1.
\nTable 2 shows 10 meat and fish products and their composition, as specified on the label. Each of the investigated items contained at least 1 of the 16 most common food additives (Table 1). As much as 50% of meat and fish products contained four or more of such additives. The highest number of additives (seven) was found in “Z doliny Karol” mortadella. “Masarnia u Józefa” crispy ham and “Lipsko” Śląska sausage contained six different food additives. Seventy percent of the examined products had had sodium nitrite (E250) added. This means that this preservative is frequently added to meat products, as confirmed in Ref. [9]. Other widespread preservatives mentioned in Ref. [9] include lactic acid (E270), sodium benzoate (E211), sorbic acid (E200), and sulphur dioxide (E220). In Ref. [9] it also mentions other additives frequently added to meat and fish products; these include carrageenan, gum arabic, and xanthan gum. In this study, 50% of the examined items contain one or two gums, and carrageenan is present in only three in ten products. A study in Ref. [17] demonstrates that fish products are the second leading food (after edible fats) in terms of preservative content.
\nProduct | \nIngredients | \nProduct | \nIngredients | \n
---|---|---|---|
Szynka krucha (ham) Masarnia u Józefa | \nPork ham, salt, pork protein, | \nPasztet podlaski (pâté) 155 g Drosed | \nWater, mechanically separated chicken meat, rapeseed oil, chicken liver and skin, cream of wheat, salt, soy protein, potato starch, dried vegetables, spices, powdered milk, (milk) whey, sugar, | \n
Kiełbasa śląska (sausage) Lipsko | \nPork 60%, pig fat 17%, water, mechanically deboned chicken meat, fibre, pork skin emulsion, potato starch, milk proteins, | \nŁuków przysmak kanapkowy (tinned meat) 300 g | \nPork meat 30%, water, beef meat 18%, pig fat, soy protein, salt, beef fat, | \n
Mortadela doliny (mortadella) Karol | \nWater, pork 20%, mechanically separated chicken meat 15%, pig fat, pork connective tissue, cream of wheat, acetylated starch, polyphosphates, | \nAgrovit duże porcje konserwa tyrolska (tinned meat) 400 g | \nWater, mechanically separated chicken meat 23%, pork raw materials 23%, modified (corn) starch, wheat fibre, pea fibre, salt, | \n
Mięso mielone wieprzowe (ground pork) Adrian | \nPork meat 65%, pig fat 34%, salt, | \nEuro Fish szprot w sosie pomidorowym (sprat in tomato sauce) 170 g | \nFish—sprat without heads—tomato sauce, water, tomato concentrate, sugar, rapeseed oil, salt, modified starch, dried onion, | \n
Parówki (frankfurters) Indykpol | \nChicken meat 25.9%, mechanically separated turkey meat 17%, mechanically separated chicken meat 17.3%, water, poultry fat, pork, corn flour, chicken skins, pig fat, pork skins, potato starch, soy protein, salt, spices, spice extracts, flavourings | \nGraal Flet z makreli w sosie pomidorowym (mackerel fillet in tomato sauce) 170 g | \nMackerel fillets 60%, tomato sauce, water, tomato concentrate, sugar, rapeseed oil, modified starch, spirit vinegar, salt, powdered tomatoes, dried onion, spice extract, spices, | \n
Food additives and ingredients in the studied meat and fish products.
Table 3 shows ten non-alcoholic beverages, six of which contain at least one common food additive (Table 1). Foreign substances that are most frequently found in this food group are citric acid (E330), sodium benzoate (E211), and glucose-fructose syrup. A study in Refs. [18, 19] shows that the most popular sweeteners in non-alcoholic beverages are glucose, fructose, and glucose-fructose syrups. As shown on product label, 100% juice by brands such as “Hortex” and “Tymbark”, as well as “Cisowianka” and “Kubuś” mineral waters, is additive free. Pursuant to the Regulation of the European Parliament and of the Council (EC) of 16 December 2008, no food additives may be used in mineral and spring bottled water. The beverage to contain the largest number of additive substances was white orangeade by “Hellena”.
\nProduct | \nIngredients | \nProduct | \nIngredients | \n
---|---|---|---|
Woda mineralna gazowana (carbonated mineral water) Cisownianka 1.5 L | \nNatural mineral water, unsaturated with carbon dioxide, moderately mineralised | \nWoda mineralna niegazowana (non-carbonated mineral water) Kubuś water 0.5 L | \nWater, cane sugar, apple juice from concentrated apple juice, lemon juice from concentrated lemon juice, flavouring | \n
Sok jabłko (apple juice) 100% 1 L Hortex | \n100% apple juice from concentrated apple juice | \nCoca cola 1.5 L | \nWater, sugar, carbon dioxide, | \n
Sok multiwitamina (multivitamin juice) 100% 1 L Tymbark | \nJuices from concentrated apple juice 60% and orange juice 22%, carrot juice from concentrated juice 12%, purées from banana 3%, peach, guava, papaya, juices from concentrated pineapple juice 2%, mango juice 0.5%, passion fruit juice 0.1%, lychee juice 0.05%, cactus fig juice, kiwi fruit juice and lime juice, vitamins A, C, E, B6, and B12, thiamine, riboflavin, niacin, biotin, folic acid, pantothenic acid | \nTymbark 2 L jabłko-pomarańcza (apple-orange) | \nWater, orange juice from concentrated juice 19%, | \n
Volcano 2 L cola | \nSpring water, carbon dioxide, sulphite ammonia caramel, phosphoric acid, | \nVolcano 2 L pomarańcza (orange) | \nSpring water, carbon dioxide, orange juice 0.3% from concentrated orange juice, | \n
Hellena 1.25 L oranżada biała (white orangeade) | \nSugar, water, | \nKubuś marchew, jabłko, pomarańcza, sok (carrot, apple, and orange juice) 330 mL | \nPurées and juices (59%), water, | \n
Food ingredients in the studied non-alcoholic beverages.
Table 4 shows 12 food items, such as ketchup, mustard, herbs and spices, and tomato concentrates, together with their composition. Only four products in this group contain a food additive, of which three are preserved using citric acid (E330). In this group of products, the products to contain the most common additive substances were the ketchup and the Kucharek seasoning by “Prymat”. Pursuant to the Regulation of the European Parliament and of the Council (EC) of 16 December 2008, tomato products (such as concentrates) must not contain food colours. They may, however, contain other additives. The ketchup has no colours, but contains other food additives. Studies in Ref. [17] demonstrate that mayonnaises and mustards are the fourth most often preserved product group, with ready-made concentrates ranking seventh. One of the two mustards examined in this paper contained a preservative, and two of the presented tomato concentrates had not had any food additives added to them.
\nProduct | \nIngredients | \nProduct | \nIngredients | \n
---|---|---|---|
Koncentrat pomidorowy (tomato concentrate) Aro 190 g | \n30% tomato concentrate | \nKoncentrat pomidorowy (tomato concentrate) Pudliszki | \n30% tomato concentrate | \n
Ketchup łagodny (mild ketchup) 470 g | \n37% tomato concentrate, water, sugar, vinegar, modified starch, salt, | \nKetchup Pudliszki łgodny (mild ketchup) 480 g | \nTomatoes, sugar, vinegar, salt, modified starch, natural flavouring | \n
Musztarda Parczew kremska (Krems mustard) 180 g | \nWater, mustard seeds, vinegar, sugar, salt, spices | \nMusztarda Roleski stołowa (table mustard) | \nWater, mustard seeds, sugar, spirit vinegar, salt, spices, turmeric extract, | \n
Zioła prowansalskie (Herbes de Provence) Prymat | \nBasil, marjoram, rosemary, savoury, sage, thyme, oregano, mint | \nPrzyprawa do kurczaka (chicken seasoning) Goleo | \nSalt, garlic, white mustard seeds, sweet pepper, carrot, coriander, fenugreek, caraway, chilli, turmeric, cinnamon | \n
Przyprawa Tzatziki (tzatziki seasoning) Prymat | \nGarlic, salt, sugar, onion, | \nKucharek Prymat 250 g | \nSalt, died vegetables, | \n
Food ingredients in the studied condiments.
Table 5 shows 12 products categorised into ready-made dishes, soups and sauces, and their chemical composition. Each of these products contains at least one common additive. Citric acid (E330) was added to nearly 67% of the products in this category. Only five in twelve items (including four instant soups and stock cubes) contain the three most popular food additive substances (Table 1). A study in Ref. [13] shows that the most common additives in ready-made dishes are citric acid (E330), sunset yellow (E110), guar gum (E412), disodium guanylate (E627), disodium inosinate (E631), and monosodium glutamate (E621).
\nProduct | \nIngredients | \nProduct | \nIngredients | \n
---|---|---|---|
Rosół drobiowy kucharek (chicken soup) 60 g | \nSalt, palm fat, partially hydrogenated, starch, | \nRosół drobiowy Winiary (chicken soup) 60 g | \nSalt, | \n
Vifon kurczak Carry (curry chicken) | \nNoodles (92.1%), wheat flour, plant fat, tapioca, modified starch, acetylated starch, sugar, stabilisers (pentasodium triphosphate, | \nAmino zupa błyskawiczna gulaszowa (instant goulash soup) | \nNoodles (85%), wheat flour, palm fat, modified starch, salt, rapeseed oil, | \n
Sos Winiary Italia boloński (Bolognese sauce) | \nDried vegetables, modified starch, sugar, salt, spices, flavourings, sunflower oil, | \nSos Winiary pieczeniowy ciemny (dark roasting sauce) | \nPotato starch, modified starch, salt, dried vegetables, flavourings, sugar, yeast extracts, fully hydrogenated palm fat, palm oil, rice flour, | \n
Sos Winiary borowikowy (bolete sauce) | \nCorn starch, wheat flour, powdered cream, palm oil, sunflower oil, | \nZupa Winiary barszcz biały (white borscht) | \nWheat flour, skimmed powdered milk, salt, potato starch, sugar, smoked pig fat, citric acid, dried vegetables, yeast extract, herbs, spices, smoke flavour | \n
Zupa Winiary jak u mamy pieczarkowa (champignon soup) | \nCorn starch, skimmed powdered milk, wheat flour, powdered cream, dried champignons, yeast extracts, salt, potato starch, dried vegetables, flavourings, sunflower oil, wheat protein hydrolysate, parsley, black pepper, | \nŁowicz sos boloński (Bolognese sauce) 350 g | \nTomatoes, water, vegetables, | \n
Danie gotowe Flaczki (ready-made tripe) Pamapol | \nWater, beef rumen 305, wheat flour, carrot, parsley, celeriac, tomato concentrate, onion, salt, pork gelatine, sugar, soy protein hydrolysate, dried vegetables, yeast extract, spices, | \nPomysł na soczystą karkówkę z ziemniakami (pork shoulder with potatoes seasoning) Winiary | \nWheat flour, vegetables, salt, modified starch, yeast extract, herbs, | \n
Food ingredients and additives in the studied ready-made dishes, soups, and sauces.
Table 6 shows 10 food items classified as sweets and desserts. As many as nine products in this group contained at least one of the most common food additives (Table 1). Glucose-fructose or glucose syrups were found in six of the examined items. A study in Ref. [19] shows that sweets often include the so-called Southampton colours, such as quinoline yellow and tartrazine. However, the study reports that the amounts of these substances added to sweets are much lower than the maximum values allowed by the applicable law.
\nProduct | \nIngredients | \nProduct | \nIngredients | \n
---|---|---|---|
Lód Top milker (ice cream) Koral | \nSkimmed reconstituted milk, sugar, cocoa oil, | \nBaton 3bit (candy bar) | \nSugar, biscuit 14% [wheat flour, sugar, plant fat, powdered whey, | \n
7 days | \nWheat flour, cocoa filling 25% [(sugar, partially hydrogenated plant fats, water, low-fat powdered cocoa 7%, skimmed powdered milk, ethyl alcohol, emulsifier (lactic acid esters of mono- and diglycerides of fatty acids), vanilla flavouring, gelling agent (sodium alginate), preservative (potassium sorbate 0.1%)], margarine [partially hydrogenated plant fats, water, salt, emulsifier (mono- and diglycerides of fatty acids), acidity regulator, flavouring, preservative (potassium sorbate 0.1%)], sugar, stabiliser (mono- and diglycerides of fatty acids), | \nLód rożek truskawkowy (ice cream cone) Koral | \nSkimmed reconstituted milk, cornet 14% [wheat flour, sugar, palm fat, potato starch, emulsifier ( | \n
Baton Milky way (candy bar) | \nSugar, | \nMlekołaki Lubella muszelki (cereal) 250 g | \nWholemeal wheat, wheat, and corn flours, sugar, glucose, reduced-fat cocoa, cocoa, barley malt extract, milk chocolate, palm fat, salt, | \n
Nestlé Corn Flakes 600 g | \nCorn grits, sugar, salt, glucose, brown sugar, invert sugar syrup, cane sugar molasses, sodium phosphates, niacin, pantothenic acid, riboflavin, vitamin B6, folic acid | \nNestlé Frutina 250 g | \nWheat flakes (wholemeal wheat, sugar, wheat bran, barley malt extract, invert sugar syrup, salt, cane sugar molasses, | \n
Lays zielona cebulka (crisps) 150 g | \nPotatoes, palm oil, sunflower oil, flavouring, powdered onion, powdered milk whey, powdered milk lactose, sugar, powdered milk, | \nStar chips paprika (crisps) 170 g | \nPotatoes, palm fat, flavourings, wheat breadcrumbs, glucose, sugar, | \n
Food additives and ingredients in the studied sweets.
A commonly found preservative is
A common ingredient in food is
What frequently occurs in consumer goods is
Another frequently added substance is
The most widespread natural emulsifier is
Common preservatives include benzoic acid and its salts, of which the most frequently used is
The external aspect that is most crucial for buyers when it comes to food selection is its freshness. Buyers assess the best before date against the possibility of consuming the food quickly or storing it for future use. Another determinant is the value of the item. Any consumer will pay attention to the price of the product they buy. Another factor is the product ingredients specified on the packaging. Buyers have been observed to have developed a habit of reading labels before buying anything. Some customers also pay attention to the country of origin or brand [22]. Men and women who are determined to stay fit will also consider nutritional value. The factors that are not considered that are relevant include net product weight, information about any genetically modified raw material content, and notices about any implemented quality management systems. Moreover, consumers are likely to be affected by marketing devices, such as advertisements or special offers, used by producers. A temporary reduction in price, or the opportunity to buy two items for the price of one, encourages customers to make a purchase [3, 4]. What is also vital is whether the food is functional. Many people live at a fast pace, work a lot, or get stuck in traffic jams, and the lack of free time pushes them to buy ready-made dishes to be heated up at home or food that can be prepared in an instant [4, 13, 22].
\nNowadays, food additives are very widespread in the everyday human diet, but not all of them are synthetic and invasive to human health. Products which must not contain foreign substances do not contain food additives. The explorations undertaken by this and other studies confirm the widespread use of the investigated additives, except for citric acid, which is less popular an additive than sodium benzoate and potassium sorbate. This study shows that when adopting a healthy lifestyle, consumers can choose from a range of food and pharmaceutical products that either contain a limited amount of unconventional substances or do not contain such substances at all.
\nReactive oxygen species (ROS) are known to determine oxide-reducing balance alteration, oxidative stress, and carcinogenicity. Many diseases, including cancer and other pathologies associated, like arteriosclerosis and cataracts, are related to mitochondrial dysfunctions provoked by reactive oxygen species [1, 2]. Free radicals (O2−, HO•, H2O2) react easily and cause damage to the DNA and cell membranes, generating strong oxidant agents inside cells [3]. Reactive oxygen species (ROS) play a role in a number of degenerative conditions including osteoporosis [4].
\nBone is an important organ performing three essential physiological functions: mechanical support, mineral homeostasis, and support of hematopoiesis. Bone diseases in the elderly are associated with increased morbidity and mortality. Osteoporosis is one of the most important diseases that affects the quality of life for the elderly [5]. Although the bones stop growing after adolescence, the bone is a very dynamic tissue. Bone tissue is continuously reabsorbed and regenerated by constantly changing its structure.
\nOne of the most striking features of the bones is their ability to reshape. This remodeling process occurs during growth and continues throughout its life. During bone formation, the bone is formed and deposited, according to a particular pattern, by a process called ossification. The remodeling is continuous, leading to the organization of the bone structure in regular units, allowing the bone mass to gain maximum resistance to the mechanical forces acting on it. The older bone is removed by osteoclasts (bone-resorbing cells), and osteoblasts (bone-forming cells) lead to the deposition of new bone tissue. Osteoclasts secrete enzymes that break down the bone matrix as effectively as acids and convert calcium salts resulting in a soluble form (that can be absorbed into the bloodstream).
\nOsteoclast activity occurs behind the epiphyseal growth zone to reduce bone margins enlarged at the width of the bone stem that undergoes an elongation process.
\nThe remodeling process is especially important for long bones supporting the limbs. These bones are widest at the ends and narrower in the middle, which gives added strength to the joints.
\nAs osteoclasts destroy the old bone at the epithelial ends of the bone, the osteoblasts within the growth zone create a new epiphysis.
\nIn each of the tubular spaces released by osteoclasts within the bone, the osteoblasts come in to deposit a new bone layer.
\nA bone that is poorly used, such as a lower immobilized member after a trauma, will be prone to reabsorption because bone destruction goes beyond bone formation.
\nBones subjected to increased stress are permanently remodeled. The femur, for example, is completely replaced every 6 months.
\nBone remodeling gives the different form of long bones. They are wider at each end and thinner in the middle. Bone remodeling not only changes the bone structure but also helps regulate the level of ionic calcium in the blood. Calcium is necessary for normal nervous transmission, for cell membrane formation, and for blood clotting. The resorption and bone formation sequence is shown in Figure 1.
\nBone remodeling sequence executed by different bone cell types within basic multicellular units (BMUs) (figure from Ref. [
Osteoblasts (bone-forming cells), osteoclasts (bone-resorbing cells), and osteocytes (load-sensing cells) are the cell types participating in bone remodeling. During remodeling, these cell types are spatially and temporally organized in functional structures called basic multicellular units (BMUs). The remodeling sequence operated by a BMU follows well-defined phases [5]. The bone remodeling sequence is influenced by a number of regulatory factors produced by hormonal glands, bone cells involved in sensing the mechanical environment, lymphocytes, and even tumor cells [6].
\nOsteoporosis is characterized by the parallel reduction of bone minerals and bone matrix so that the bone is in a low amount but with a normal percentage composition.
\nDespite rapid advances in our understanding over the last few years, the morbidity and mortality of patients resulting from this disease are still too high [4], and there is an urgent need for a proper assessment of the underlying mechanisms and the development of new treatment strategies to address this pathophysiological issue.
\nOxygen (O2), nitrogen oxide (NO), and iron (Fe2+) are present in erythrocytes. These elements may in some conditions form reactive species, called radicals that affect red blood cells and vascular endothelium. A chemical species that presents an unpaired electron in outer orbitals and which can exist independently is called free radical. Radicals are very reactive trying to complete their own orbits by taking an electron from a neighboring molecule. Oxygen and nitrogen are the two chemical elements that in the body give rise to reactive species called the reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively.
\nReactive species can be defined as atoms or molecules that contain in their structure an odd electron that causes an atom/molecule energy instability, which is reflected in their increased reactivity.
\nReactive species are produced in the body for physiological purposes in defense, vaso-relaxation, cellular or accidental exposure to toxic, or radiation exposure. When the amount of reactive species exceeds nontoxic physiological levels, the so-called oxidative stress occurs. Oxidative stress can be defined as the status of reactive oxygen or oxygen radicals in a biological system. It results from the imbalance between oxidants and antioxidants, in favor of oxidants, with destructive and pathogenic potential [7, 8].
\nThe reactive species of oxygen are superoxide (O2•−), hydrogen peroxide (H2O2), hydroxyl radical (OH•), and singlet oxygen (1O2). Free oxygen radicals (ROS) produce harmful effects on the body called oxidative stress (OxS). The reactive oxygen species are constantly formed as reaction products in all cells by aerobic processes such as oxidative phosphorylation.
\nThe base state of oxygen is triplet. This means that it has two unpaired electrons that are positioned on two different molecular orbitals.
\nBecause electrons have parallel spin, oxygen can only rotate in the same orbit. Since molecular oxygen is paramagnetic, it is concluded that it has the structure represented in the right-hand side of Figure 2. Molecular oxygen can react rapidly with single unpaired electrons of transitory metals (e.g., Fe, Cu, Mn). One mole of properly chelated copper could catalyze consumption of the oxygen in an average room within 1 s in [9]. Depending on the conditions, O2 can be both kinetically stable (not reactive) and very reactive.
\nThe structure of oxygen molecule.
For proteins and enzymes that have a metal in their structure, the oxidative attack of O2 is slow, and in conclusion the superoxide radical will slowly form.
\nSuperoxide (O2): this radical constitutes the first step of oxygen activation by way of univalent reduction, forming in most of the autoxidation reactions by the capture of an electron that is placed on one of the antiknocking orbital n (Figure 3).
\nSuperoxide radical generation.
After an electron has been acquired, the following electrons are added more easily, and the reactions take place faster, leading to the generation of reactive oxygen species [10].
\nReducing the hydroxyl radical to water takes place in the last stage of electron acceptance (Figure 4).
\nReactive oxygen species generation.
Superoxide radical (O2) can react in the presence of ferric iron with hydrogen peroxide generating the most potent hydroxyl radical through a nonenzymatic reaction named Haber-Weiss reaction.
\nThe reaction involves two steps:
\nThe nonenzymatic reaction occurring in living cells is:
\nIn the presence of ferric iron, superoxide radical is a source of hydroxyl radical.
\nMost of the superoxide radicals are formed by electrons derived from the coenzyme Q cycle in complex III and by NADH flavoprotein dehydrogenase (complex I). The superoxide radical, which has a relatively low degree of toxicity compared to other reactive oxygen species, is kept undetected by enzymes called superoxide dismutase (SOD) that catalyzes the dismutation reaction.
\nSinglet oxygen can be formed from superoxide radical in [11]:
\nAlthough it is not a radical, singlet oxygen is more reactive than the hydroxyl radical. The most reactive radical is hydroxyl (OH•) which takes electrons from other molecules around it, whereas superoxide (O2) and hydrogen peroxide (H2O2) are more selective in their reactions with various molecules [12].
\nThe processes so far presented above take place in all human cells. The molecular oxygen that is transported to the tissues is found for a short period of time unbound. It is assumed that in this state, it generates the radicals previously presented. Oxygen binds to hemoglobin molecule at the ferrous iron (Fe2+). Some of Fe2+ is transformed by O2 to ferric form (Fe3+) in resulting methemoglobin. Methemoglobin reductase is an enzymatic system which restores Fe3+ to Fe2+ and reduces methemoglobin back to hemoglobin. Oxygenated hem has some of the electronic characteristics of a Fe3+OO peroxide anion [10]. Like in this study [13], the author found that the Fe3+O2− complex is able to generate superoxide radical during the normal molecular oxygen transport to tissues through the hemoglobin auto-oxidation.
\nSome researchers propose that hemoglobin may have oxidative reaction in the oxygen-releasing process.
\nLike in this study from 2006 [14], the author demonstrates that at intermediate oxygen pressure, where hemoglobin partially releases molecular oxygen, the superoxide radical production increases. They show that superoxide radical is released in the hydrophobic hem pocket.
\nThrough the Haber-Weiss reaction, H2O2, even if it is not a radical, can form short and very active hydroxyl radicals [15]. The hydroxyl radical (OH•), which is highly reactive, reacts with any biomolecules it encounters. There are studies according to which the high reactivity of the hydroxyl radical decreases its ability to diffuse [16]. Since the hydroxyl radical may generate an autocatalytic reaction in the chain, we can say that it is particularly dangerous.
\nThere are some researchers who believe that the hydroxyl radical is responsible for cellular damage and others that ferric ion promotes initiation of the chain reaction [17, 18, 19]. In conclusion, both oxidative species can form in living cells [20].
\nLike in Figure 4, ROS are produced accidentally and physiologically in various enzyme-catalyzed reactions.
\nReactive oxygen species can interact with any biological molecule causing damage to lipids, proteins, and DNA. Prospects for effective therapeutic intervention may fail if the initial target of oxidative stress is unknown. For example, it is known that DNA is the primary target of lesions produced by the addition of H2O2 to mammalian cell cultures, so that DNA strand breaks occur before lipid peroxides or “detectable” oxidized proteins. The method of detecting lesions produced on target molecules may give incomplete information. The evidence of protein damage by detecting carbonyl radicals in the initial stages of lesions may be negative, but the determination of SH oxidation, which occurs earlier, is positive. During peroxidation of lipids, the peroxyl radicals are formed by chain reactions. These intermediates that are formed can amplify the lesion. The attack of ROS affects both erythrocytes and endothelial cells. DNA damage may occur in nucleus containing endothelium cell besides lipid and protein oxidation. Interaction between free radicals and DNA can lead to strand breaks or structural changes such as adduct formation (Figure 5) [21, 22].
\nROS damaging activity.
In general, lipid peroxidation occurs in late stages of aggression, so therapies directed against lipoperoxidation may be less beneficial. This is another reason that can lead to erroneous conclusions about the importance of oxidative stress and antioxidant therapies.
\nAs long as they do not accumulate in excess, ROS have positive effects in the body, being involved in various cellular mechanisms. For example, biosynthesis of thyroid hormones involves the formation of hydrogen peroxide in order to assemble thyroglobulin iodine to synthesize thyroxine. On the other hand, in the immune response, in neutrophils and macrophages, NADPH oxidase catalyzes the formation of superoxide anion by internalizing bacterial antigenic structures. The process is completed by the action of SOD, which will produce hydrogen peroxide that will induce bacterial lysis. It has been shown that ROS acts as a signaling molecule [21, 22]. In response to the intensity of attack of the ROS, cellular responses are triggered, which prepare the cells to survive or to die (Figure 6).
\nCells response under ROS attack [
Oxidative stress can trigger cellular response through different signaling modes. ROS modulates different types of enzymes, the activity of transcription factors, and the ionic channel. Both kinases and phosphatases can be modulated by ROS.
\nMitogen-activated protein kinase (MAPK), which has three subfamilies, namely, N-terminal c-Jun kinase (JNK), p38 MAPK, and extracellular signal-regulated kinase (ERK), is part of the kinase class [24]. These MAPK pathways are structurally the same. The difference between them is found at a functional level. ROS activates these three MAPK pathways [25] and may inhibit tyrosine phosphatase activity.
\nIn gene and protein expression, ROS are involved by activating transcription factors.
\nThe plasma membrane Ca2+ and K+ channels are stimulated by ROS. The increase in calcium ion concentration ROS mediated leads to the oxidative stress-mediated activation of PKC and to the transcriptional induction of the AP-1 proteins c-Fos and c-Jun [26].
\nCells can be protected from attack by reactive species through various mechanisms. Antioxidants can be divided into two groups: enzymatic like superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase and nonenzymatic like vitamins E and C, provitamin A (b-carotene), and glutathione.
\nSOD is found in all aerobic cells as well as in aerobic optional bacteria. Initially, it was interpreted as a copper storage form, and later three types of SODs were described, based on the type of metal in the catalyst center.
\nThe role of superoxide dismutase is to catalyze the dismutation reaction of the superoxide radical anion according to the equation (Figure 7):
\nSuperoxide dismutase activity.
The enzyme may also inhibit the production of singlet oxygen and indirectly the peroxidation of polyunsaturated fatty acids. In addition to the role of the oxidative marker, SOD is tested as a potential therapeutic agent under pathological conditions in which the oxidative stress has a clear role, such as ischemia-reperfusion syndromes, hepatic disorders and acute and chronic inflammation, cataracts, rheumatic arthritis, diabetes, and neoplasia. One of the enzyme-catalyzed reactions leads to the appearance of another harmful compound—hydrogen peroxide [27].
\nGPx is part of a family of enzymes catalyzing the degradation of H2O2 resulting from normal metabolic processes and providing the protection of proteins, lipids, and nucleic acids from the action of oxidizing molecules, using glutathione as an electron donor or, in some cases, thioredoxin or glutaredoxin (Figure 8).
\nGlutathione peroxidase activity.
GPx is a dependent selenium enzyme, found in cytosol (70%) and in mitochondria (30%). It is irreplaceable in the antioxidant arsenal, especially in mitochondria, as they do not contain catalase for peroxide metabolism. GPx also provides protection against organic H2O2 and helps to regenerate the reduced vitamin C form. Imbalances in the GPx level have been observed with aging and a variety of disorders such as cancer, cardiovascular disease, and diabetes [28].
\nGPx is an enzyme that has a potentially greater antioxidant than SOD and catalase due to the wide-specific substrate. Other roles of GPx are regulating prostaglandin biosynthesis by inhibiting lipoxygenase and, in conjunction with glutathione reductase, contributing to the restoration of reduced glutathione.
\nBone tissue undergoes, throughout life, a continuous renewal through a process called bone remodeling, which is controlled by the activity of osteoclasts mediating bone resorption and parallel activity of osteoblasts which mediate bone formation [29]. A bone remodeling cycle involves three stages: (1) initiation, during which osteoclasts are formed and resorb damaged bone; (2) reversal, the transition of osteoclast to osteoblast activity; and (3) formation, when osteoblasts replace the portion of the bone that was resorbed [30]. The hormonal imbalance or the aging process can lead to disruption of the balanced formation process and bone resorption. This may result in decreased bone mass and osteoporosis, which increases the risk of fractures. A very important factor underlying the pathogenesis of osteoporosis is the receptor activator of NF-κB ligand (RANKL). It plays an important role in osteoclast differentiation and activation [31]. For this reason, inhibition of RANKL represents an innovative therapeutic target for controlling osteoclastogenesis [32].
\nIn the bone remodeling process, the alternative NF-κB pathway, which mediates the activation of the p52/RelB NF-κB complex, is involved. The difference of the alternative mechanism is represented by p100 processing of a NF-κB2 precursor protein. Both NF-κB-inducing kinase (NIK) and IKKα, a downstream kinase, promote induction of phosphorylation-dependent ubiquitination for p100. NF-κB-inducing kinase is processed by a tumor necrosis factor (TNF) receptor-associated factor-3 (TRAF3)-dependent E3 ubiquitin ligase. NIK activates the alternative path of NF-kB. This occurs after signals mediated by a subset of TNF receptor superfamily members [33]. The inhibitory role of p100, in both basal and stimulated osteoclastogenesis in bone formation and resorption, has been clearly demonstrated [34]. In the alternative NF-κB pathway p52 derived from p100 through NIK, binding of p52 and RelB induces effects on osteoclast biology [34]. However, to date, the precise physiologic importance of alternative NF-κB in bone biology is not completely elucidated. Furthermore, the currently known intracellular signaling pathways activated after receptor binding of RANKL include the nuclear factor of activated T cells [35], mitogen-activated protein kinases (MAPKs), TRAFs, c-Jun N-terminal kinases (JNKs), and ROS [36, 37]. In addition, NF-κB is a transcription factor, which pleiotropically regulates osteoclast formation, function, and survival [35].
\nThe reactive oxygen species are involved in the regulation of RANKL-dependent osteoclast differentiation. They act as intracellular signaling compounds. ROS have cytotoxic effects, including lipid peroxidation and DNA damage.
\nSince the relationship between Nrf2 and osteoclastogenesis is known, stimulation of precursors of osteoclasts with RANKL will lead to the upregulation of Keap1 and downregulation of cytoprotective enzymes. Osteoclast precursors are primary peritoneal macrophages and RAW 264.7 cells. Keap 1 is a negative regulator of Nrf2. However, overexpression of Nrf2 leads to the regulation of the expression of heme oxygenase-1 and gamma-glutamylcysteine synthetase enzymes associated with decreased reactive oxygen species and slowing of bone destruction [38]. Consistent with this line of evidence, overexpression of Keap1 or RNAi-induced knockdown of Nrf2 resulted in effects opposite to those obtained by stimulation of Nrf2-dependent DNA binding activity [38]. We still do not know the exact mechanisms by which RANKL stimulation reduces Nrf2. It is known that Keap1 has in its structure thiol groups. These groups are highly reactive, and oxidation at their level produces conformational changes to Keap1. Ultimately these will lead to dissociation from Nrf2 and promotion of nuclear Nrf2-dependent DNA binding activity [38].
\nIn addition, Nrf2 autoregulates its own expression [39, 40, 41]. Taken together, this evidence implies that an increase in ROS levels induced by stimulation with RANKL may upregulate Nrf2. It has also been reported that Nrf2 regulates Keap1 by controlling its transcription [39, 40, 41].
\nDecreasing translation through miRNA can modulate downregulation of Nrf2. The downregulation of Nrf2 may be modulated by decreasing translation by miARN or by modifying the mRNA stability Nrf2. Bach1 is an inhibitor of Nrf2 binding to ARE. This inhibitor is implicated in the mechanism indicated by the inhibited osteoclastogenesis discovered in Bach1 knockout mice [38]. In conclusion, the Keap1/Nrf2 axis regulates RANKL-dependent osteoclastogenesis both by modulating intracellular ROS signals and by expressing cytoprotective enzymes. Elucidation of the precise mechanism linking Nrf2 to stimulation with RANKL may be a therapeutic treatment for destructive bone disorders through the Keap1-Nrf2 axis [42].
\nThe human aging implies a failure in bone formation and a loss of bone mass, but the specific molecular mechanisms arbitrating these effects are still unclear. Numerous studies in experimental animals have offered arguments for a damaging effect of oxidative stress in bone tissue, supporting the idea that an increase in reactive oxygen species (ROS) with advancing age characterizes a pathophysiological mechanism essential in age-related bone damage. The disproportion between bone resorption and formation with age is related to various factors. A reduced wall width represents the most common histological feature in aged human bone due to a reduced deposition of bone matrix related to an insufficient number of osteoblasts involved in bone remodeling [43, 46]. It was found that the low number of osteoblasts in the aging bone is correlated with a decrease in the number of mesenchymal stem cells and improper proliferation and differentiation of progenitor cells [45]. An additional histologic feature of aged human bone tissue is a decrease in osteocyte density in the structure of bone lamellae accompanied by a mineralization of osteocyte lacunae. The precise mechanism of this phenomenon—named micropetrosis—is not very well known, but it seems to contribute to the decrease in osteocyte density with age [44, 45, 46].
\nThe histopathological examination reveals thinned bone trabeculae that lose continuity being separated from each other by enlarged areolae with adipose degeneration of the marrow. The reduction of the trabecular connectivity is related to osteoporosis stages. The decrease of the medullar cellularity together with its enhancement in fat cells has negative outcomes on the bone. The areolar spaces are stretched, bordered by incomplete bone septa. This fact could be explained by the decrease of the connectivity of the bone trabeculae that will lead to the connection of the areolae by the osteolysis of certain walls (Figures 9 and 10).
\nOsteoporotic bone—hematoxylin-eosin (HE) stain.
Osteoporotic bone—trichromic Goldner-Szekely stain.
Healthy people have a balance between bone formation and bone resorption. In various bone diseases, even in malignancy, loss of this balance leads to damage to the normal structural integrity of the skeleton [47, 48]. Tumor cells act by excessive stimulation of both osteoclasts and osteoblasts.
\nOxidative stress is one of the most important events that gives rise to the conditions leading to tumor onset and progression [49]. Reactive oxygen species (ROS) is one of the most important species of free radicals. ROS controls many cellular processes, including cell proliferation, and thus stimulates the uncontrolled cell growth which may lead to tumor development [50]. In the case of chronic inflammation, the secretion of ROS may lead to the amplification of dysregulated processes and eventually to the development of a pre-neoplastic state.
\nWhen the endogenous antioxidant response is exceeded by the amount of ROS produced, oxidative damage can occur in the lipids, proteins, and DNA. These lesions can lead to genetic alterations and ultimately to dysregulation of suppressor genes. Since oxidative stress and chronic inflammation processes are linked, failure to block these processes can lead to the initiation of carcinogenesis through genetic alterations [51]. In patients who have cancer, low total antioxidant capacity can be detected even before oncological treatment is started [52].
\nDiabetic patients have been shown to increase lipid peroxidation and decrease the activity of erythrocyte antioxidant enzymes. Hyperglycemia is due to impaired insulin secretion in T1DM and insulin resistance in T2DM.
\nIn hyperglycemic conditions, oxidative stress occurs as a result of the increased activity of the polyol pathway [53], the hexosamine pathway [54, 55, 56], and the promotion of the activator of protein kinase C [57]. Hyperglycemia also leads to a higher activation of the nuclear-kappa B (NF-κB), by protein kinase C in vitro. The nuclear factor-kappa B is a central transcription factor involved in the regulation of many proinflammatory genes, including cytokines (TNF-tumor necrosis factor, interleukin) and hematopoietic growth factors [58]. Under hyperglycemic conditions, the NADH/NAD + cytosolic ratio increases because sorbitol is oxidized by NAD +. In this situation, the activation of the glyceraldehyde-3-phosphate dehydrogenase enzyme is inhibited. Although there is still little research, type 1 diabetes has been associated with osteoporosis. Therefore, we can say that type 1 diabetes may increase the risk of fractures [59]. Type 1 diabetes affects both bone density and bone quality [60, 61]. In T2DM, BMD is equal or increased according a meta-analysis, but the fracture risk is increased despite this increase in BMD [62, 63].
\nOsteocalcin (OST) is the second structural protein after collagen, a component of bone tissue, mainly involved in the process of bone mineralization and calcium homeostasis. It is synthesized by osteoblasts, under the action of vitamins K and D3, from a pre-pro-osteocalcin precursor made up of 98 amino acids. Clinical research has shown that serum osteocalcin levels are significantly lower in patients with type 2 diabetes, becoming normal after improved glycemic control. Osteocalcin is an independent factor associated with glucose and glycated hemoglobin for menopausal women.
\nIt has been revealed that diabetes causes a reduction in the number of osteoblasts [64]. Diabetes can affect bone-forming cells through increased apoptosis. Like in this study from 2007, authors found that AGEs induced apoptosis of osteoblasts through the MAP kinase pathway [65]. Another mechanism by which diabetes is associated with bone formation is the reduction in the expression of transcription factors involved in the regulation of osteoblast differentiation [66]. Studies in rats with diabetes showed a decrease in both alkaline phosphatase activity and the formation of the mineralized matrix [67, 68].
\nRAGE, the AGE receptor, is expressed at higher osteoblast levels in rats with diabetes, thus rendering the animals more susceptible to AGEs effects [69].
\nSome enzymes called serine kinases can be induced by oxidative stress. Their induction affects the ability of insulin to activate protein kinase B and glucose transport. When insulin action is impaired, diabetic complications may occur. In this context, the NF-κB, p38 MAPK, and JNK/SAPK pathways are sensitive to oxidative stress [70].
\nA considerable amount of evidence has accumulated indicating that metabolic and endocrine alterations caused by diabetes affect bone quantity and quality over the last decades of life [71].
\nHyperglycemia-induced oxidative stress is a major contributor in the development of long-term complications of diabetes mellitus [72, 73, 74, 75].
\nIn this chapter we discussed about the role of oxidative stress in bone pathophysiology and the possibility of ROS production being a relevant therapeutic target under certain conditions.
\nBone remodeling is a process of continuous formation and resorption occurring in specific areas of the matrix. Novel therapeutic strategies have been developed that focused on the inhibition of excessive bone resorption and promotion of bone formation process. As in this study from 2017 [47], the author proposed as osteoblast inhibitors in dexamethasone (Dex)-induced apoptosis the synthetic derivatives of benzo[1,2,5]selenadiazole (SeDs). These compounds may have a protective effect. Dex treatment leads to overproduction of ROS in the cells, DNA fragmentation, caspase-3/caspase-9 activation, p53 phosphorylation, and MAPK-pathway activation. When cells were pretreated with SeDs, these modifications were blocked, suggesting to the authors that SeDs may present a therapeutic application to antagonize osteoporosis induced by glucocorticoids [47]. Accordingly, basic research can contribute to the identification of specific pathways that can be effectively targeted by novel compounds able to treat and possibly reverse osteoporosis, particularly which occur in already chronically severed patients, such as in neurodegenerative disorders. In conclusion, we have shown that osteoclast differentiation and bone resorption are associated with the generation of ROS and oxidative stress. These data also indicate that by reducing bone resorption, antioxidants have the potential to treat osteoporosis.
\nAs this section deals with legal issues pertaining to the rights of individual Authors and IntechOpen, for the avoidance of doubt, each category of publication is dealt with separately. Consequently, much of the information, for example definition of terms used, is repeated to ensure that there can be no misunderstanding of the policies that apply to each category.
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\\n\\nIntechOpen only publishes manuscripts for which it has publishing rights. This is governed by a publication agreement between the Author and IntechOpen. This agreement is accepted by the Author when the manuscript is submitted and deals with both the rights of the publisher and Author, as well as any obligations concerning a particular manuscript. However, in accepting this agreement, Authors continue to retain significant rights to use and share their publications.
\\n\\nHOW COPYRIGHT WORKS WITH OPEN ACCESS LICENSES?
\\n\\nAgreement samples are listed here for the convenience of prospective Authors:
\\n\\n\\n\\nDEFINITIONS
\\n\\nThe following definitions apply in this Copyright Policy:
\\n\\nAuthor - in order to be identified as an Author, three criteria must be met: (i) Substantial contribution to the conception or design of the Work, or the acquisition, analysis, or interpretation of data for the Work; (ii) Participation in drafting or revising the Work; (iii) Approval of the final version of the Work to be published.
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\\n\\nCompilation - a collection of Works distributed in a Book that IntechOpen has selected, and for which the coordination of the preparation, arrangement and publication has been the responsibility of IntechOpen. Any Work included is accepted in its entirety in unmodified form and is published with one or more other contributions, each constituting a separate and independent Work, but which together are assembled into a collective whole.
\\n\\nIntechOpen - Registered publisher with office at 5 Princes Gate Court, London, SW7 2QJ - UNITED KINGDOM
\\n\\nIntechOpen platform - IntechOpen website www.intechopen.com whose main purpose is to host Monographs in the format of Book Chapters, Long Form Monographs, Compacts, Conference Proceedings and Videos.
\\n\\nVideo Lecture – an audiovisual recording of a lecture or a speech given by a Lecturer, recorded, edited, owned and published by IntechOpen.
\\n\\nTERMS
\\n\\nAll Works published on the IntechOpen platform and in print are licensed under a Creative Commons Attribution 3.0 Unported License, a license which allows for the broadest possible reuse of published material.
\\n\\nCopyright on the individual Works belongs to the specific Author, subject to an agreement with IntechOpen. The Creative Common license is granted to all others to:
\\n\\nAnd for any purpose, provided the following conditions are met:
\\n\\nAll Works are published under the CC BY 3.0 license. However, please note that book Chapters may fall under a different CC license, depending on their publication date as indicated in the table below:
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LICENSE | \\n\\t\\t\\tUSED FROM - | \\n\\t\\t\\tUP TO - | \\n\\t\\t
\\n\\t\\t\\t Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported (CC BY-NC-SA 3.0) \\n\\t\\t\\t | \\n\\t\\t\\t\\n\\t\\t\\t 1 July 2005 (2005-07-01) \\n\\t\\t\\t | \\n\\t\\t\\t\\n\\t\\t\\t 3 October 2011 (2011-10-03) \\n\\t\\t\\t | \\n\\t\\t
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The CC BY 3.0 license permits Works to be freely shared in any medium or format, as well as the reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as the source Work is cited and its Authors are acknowledged in the following manner:
\\n\\nContent reuse:
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\\n\\nContent adaptation & reuse:
\\n\\n© {year} {authors' full names}. Adapted from {short citation}; originally published under {license version} license. Available from: {DOI}
\\n\\nReposting & sharing:
\\n\\nOriginally published in {full citation}. Available from: {DOI}
\\n\\nRepublishing – More about Attribution Policy can be found here.
\\n\\nThe same principles apply to Works published under the CC BY-NC-SA 3.0 license, with the caveats that (1) the content may not be used for commercial purposes, and (2) derivative works building on this content must be distributed under the same license. The restrictions contained in these license terms may, however, be waived by the copyright holder(s). Users wishing to circumvent any of the license terms are required to obtain explicit permission to do so from the copyright holder(s).
\\n\\nDISCLAIMER: Neither the CC BY 3.0 license, nor any other license IntechOpen currently uses or has used before, applies to figures and tables reproduced from other works, as they may be subject to different terms of reuse. In such cases, if the copyright holder is not noted in the source of a figure or table, it is the responsibility of the User to investigate and determine the exact copyright status of any information utilised. Users requiring assistance in that regard are welcome to send an inquiry to permissions@intechopen.com.
\\n\\nAll rights to Books and all other compilations published on the IntechOpen platform and in print are reserved by IntechOpen.
\\n\\nThe copyright to Books and other compilations is subject to separate copyright from those that exist in the included Works.
\\n\\nAll Long Form Monographs/Compacts are licensed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) license granted to all others.
\\n\\nCopyright to the individual Works (Chapters) belongs to their specific Authors, subject to an agreement with IntechOpen and the Creative Common license granted to all others to:
\\n\\nUnder the following terms:
\\n\\nThere must be an Attribution, giving appropriate credit, provision of a link to the license, and indication if any changes were made.
\\n\\nNonCommercial - The use of the material for commercial purposes is prohibited. Commercial rights are reserved to IntechOpen or its licensees.
\\n\\nNo additional restrictions that apply legal terms or technological measures that restrict others from doing anything the license permits are allowed.
\\n\\nThe CC BY-NC 4.0 license permits Works to be freely shared in any medium or format, as well as reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as it is not used for commercial purposes. The source Work must be cited and its Authors acknowledged in the following manner:
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\\n\\n© {year} {authors' full names}. Originally published in {short citation} under {license version} license. Available from: {DOI}
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\\n\\n© {year} {authors' full names}. Adapted from {short citation}; originally published under {license version} license. Available from: {DOI}
\\n\\nReposting & sharing:
\\n\\nOriginally published in {full citation}. Available from: {DOI}
\\n\\nAll Book cover design elements, as well as Video image graphics are subject to copyright by IntechOpen.
\\n\\nEvery reproduction of a front cover image must be accompanied by an appropriate Copyright Notice displayed adjacent to the image. The exact Copyright Notice depends on who the Author of a particular cover image is. Users wishing to reproduce cover images should contact permissions@intechopen.com.
\\n\\nAll Video Lectures under IntechOpen's production are subject to copyright and are property of IntechOpen, unless defined otherwise, and are licensed under the Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license. This grants all others the right to:
\\n\\nShare — copy and redistribute the material in any medium or format
\\n\\nUnder the following terms:
\\n\\nUsers wishing to repost and share the Video Lectures are welcome to do so as long as they acknowledge the source in the following manner:
\\n\\n© {year} IntechOpen. Published under CC BY-NC-ND 4.0 license. Available from: {DOI}
\\n\\nUsers wishing to reuse, modify, or adapt the Video Lectures in a way not permitted by the license are welcome to contact us at permissions@intechopen.com to discuss waiving particular license terms.
\\n\\nAll software used on the IntechOpen platform, any used during the publishing process, and the copyright in the code constituting such software, is the property of IntechOpen or its software suppliers. As such, it may not be downloaded or copied without permission.
\\n\\nUnless otherwise indicated, all IntechOpen websites are the property of IntechOpen.
\\n\\nAll content included on IntechOpen Websites not forming part of contributed materials (such as text, images, logos, graphics, design elements, videos, sounds, pictures, trademarks, etc.), are subject to copyright and are property of, or licensed to, IntechOpen. Any other use, including the reproduction, modification, distribution, transmission, republication, display, or performance of the content on this site is strictly prohibited.
\\n\\nPolicy last updated: 2016-06-08
\\n"}]'},components:[{type:"htmlEditorComponent",content:'Copyright is the term used to describe the rights related to the publication and distribution of original Works. Most importantly from a publisher's perspective, copyright governs how Authors, publishers and the general public can use, publish, and distribute publications.
\n\nIntechOpen only publishes manuscripts for which it has publishing rights. This is governed by a publication agreement between the Author and IntechOpen. This agreement is accepted by the Author when the manuscript is submitted and deals with both the rights of the publisher and Author, as well as any obligations concerning a particular manuscript. However, in accepting this agreement, Authors continue to retain significant rights to use and share their publications.
\n\nHOW COPYRIGHT WORKS WITH OPEN ACCESS LICENSES?
\n\nAgreement samples are listed here for the convenience of prospective Authors:
\n\n\n\nDEFINITIONS
\n\nThe following definitions apply in this Copyright Policy:
\n\nAuthor - in order to be identified as an Author, three criteria must be met: (i) Substantial contribution to the conception or design of the Work, or the acquisition, analysis, or interpretation of data for the Work; (ii) Participation in drafting or revising the Work; (iii) Approval of the final version of the Work to be published.
\n\nWork - a Chapter, including Conference Papers, and any and all text, graphics, images and/or other materials forming part of or accompanying the Chapter/Conference Paper.
\n\nMonograph/Compacts - a full manuscript usually written by a single Author, including any and all text, graphics, images and/or other materials.
\n\nCompilation - a collection of Works distributed in a Book that IntechOpen has selected, and for which the coordination of the preparation, arrangement and publication has been the responsibility of IntechOpen. Any Work included is accepted in its entirety in unmodified form and is published with one or more other contributions, each constituting a separate and independent Work, but which together are assembled into a collective whole.
\n\nIntechOpen - Registered publisher with office at 5 Princes Gate Court, London, SW7 2QJ - UNITED KINGDOM
\n\nIntechOpen platform - IntechOpen website www.intechopen.com whose main purpose is to host Monographs in the format of Book Chapters, Long Form Monographs, Compacts, Conference Proceedings and Videos.
\n\nVideo Lecture – an audiovisual recording of a lecture or a speech given by a Lecturer, recorded, edited, owned and published by IntechOpen.
\n\nTERMS
\n\nAll Works published on the IntechOpen platform and in print are licensed under a Creative Commons Attribution 3.0 Unported License, a license which allows for the broadest possible reuse of published material.
\n\nCopyright on the individual Works belongs to the specific Author, subject to an agreement with IntechOpen. The Creative Common license is granted to all others to:
\n\nAnd for any purpose, provided the following conditions are met:
\n\nAll Works are published under the CC BY 3.0 license. However, please note that book Chapters may fall under a different CC license, depending on their publication date as indicated in the table below:
\n\n\n\n
LICENSE | \n\t\t\tUSED FROM - | \n\t\t\tUP TO - | \n\t\t
\n\t\t\t Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported (CC BY-NC-SA 3.0) \n\t\t\t | \n\t\t\t\n\t\t\t 1 July 2005 (2005-07-01) \n\t\t\t | \n\t\t\t\n\t\t\t 3 October 2011 (2011-10-03) \n\t\t\t | \n\t\t
Creative Commons Attribution 3.0 Unported (CC BY 3.0) | \n\t\t\t\n\t\t\t 5 October 2011 (2011-10-05) \n\t\t\t | \n\t\t\tCurrently | \n\t\t
The CC BY 3.0 license permits Works to be freely shared in any medium or format, as well as the reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as the source Work is cited and its Authors are acknowledged in the following manner:
\n\nContent reuse:
\n\n© {year} {authors' full names}. Originally published in {short citation} under {license version} license. Available from: {DOI}
\n\nContent adaptation & reuse:
\n\n© {year} {authors' full names}. Adapted from {short citation}; originally published under {license version} license. Available from: {DOI}
\n\nReposting & sharing:
\n\nOriginally published in {full citation}. Available from: {DOI}
\n\nRepublishing – More about Attribution Policy can be found here.
\n\nThe same principles apply to Works published under the CC BY-NC-SA 3.0 license, with the caveats that (1) the content may not be used for commercial purposes, and (2) derivative works building on this content must be distributed under the same license. The restrictions contained in these license terms may, however, be waived by the copyright holder(s). Users wishing to circumvent any of the license terms are required to obtain explicit permission to do so from the copyright holder(s).
\n\nDISCLAIMER: Neither the CC BY 3.0 license, nor any other license IntechOpen currently uses or has used before, applies to figures and tables reproduced from other works, as they may be subject to different terms of reuse. In such cases, if the copyright holder is not noted in the source of a figure or table, it is the responsibility of the User to investigate and determine the exact copyright status of any information utilised. Users requiring assistance in that regard are welcome to send an inquiry to permissions@intechopen.com.
\n\nAll rights to Books and all other compilations published on the IntechOpen platform and in print are reserved by IntechOpen.
\n\nThe copyright to Books and other compilations is subject to separate copyright from those that exist in the included Works.
\n\nAll Long Form Monographs/Compacts are licensed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) license granted to all others.
\n\nCopyright to the individual Works (Chapters) belongs to their specific Authors, subject to an agreement with IntechOpen and the Creative Common license granted to all others to:
\n\nUnder the following terms:
\n\nThere must be an Attribution, giving appropriate credit, provision of a link to the license, and indication if any changes were made.
\n\nNonCommercial - The use of the material for commercial purposes is prohibited. Commercial rights are reserved to IntechOpen or its licensees.
\n\nNo additional restrictions that apply legal terms or technological measures that restrict others from doing anything the license permits are allowed.
\n\nThe CC BY-NC 4.0 license permits Works to be freely shared in any medium or format, as well as reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as it is not used for commercial purposes. The source Work must be cited and its Authors acknowledged in the following manner:
\n\nContent reuse:
\n\n© {year} {authors' full names}. Originally published in {short citation} under {license version} license. Available from: {DOI}
\n\nContent adaptation & reuse:
\n\n© {year} {authors' full names}. Adapted from {short citation}; originally published under {license version} license. Available from: {DOI}
\n\nReposting & sharing:
\n\nOriginally published in {full citation}. Available from: {DOI}
\n\nAll Book cover design elements, as well as Video image graphics are subject to copyright by IntechOpen.
\n\nEvery reproduction of a front cover image must be accompanied by an appropriate Copyright Notice displayed adjacent to the image. The exact Copyright Notice depends on who the Author of a particular cover image is. Users wishing to reproduce cover images should contact permissions@intechopen.com.
\n\nAll Video Lectures under IntechOpen's production are subject to copyright and are property of IntechOpen, unless defined otherwise, and are licensed under the Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license. This grants all others the right to:
\n\nShare — copy and redistribute the material in any medium or format
\n\nUnder the following terms:
\n\nUsers wishing to repost and share the Video Lectures are welcome to do so as long as they acknowledge the source in the following manner:
\n\n© {year} IntechOpen. Published under CC BY-NC-ND 4.0 license. Available from: {DOI}
\n\nUsers wishing to reuse, modify, or adapt the Video Lectures in a way not permitted by the license are welcome to contact us at permissions@intechopen.com to discuss waiving particular license terms.
\n\nAll software used on the IntechOpen platform, any used during the publishing process, and the copyright in the code constituting such software, is the property of IntechOpen or its software suppliers. As such, it may not be downloaded or copied without permission.
\n\nUnless otherwise indicated, all IntechOpen websites are the property of IntechOpen.
\n\nAll content included on IntechOpen Websites not forming part of contributed materials (such as text, images, logos, graphics, design elements, videos, sounds, pictures, trademarks, etc.), are subject to copyright and are property of, or licensed to, IntechOpen. Any other use, including the reproduction, modification, distribution, transmission, republication, display, or performance of the content on this site is strictly prohibited.
\n\nPolicy last updated: 2016-06-08
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I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. 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After obtaining a Master's degree in Mechanical Engineering, he continued his PhD studies in Robotics at the Vienna University of Technology. Here he worked as a robotic researcher with the university's Intelligent Manufacturing Systems Group as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and most importantly he co-founded and built the International Journal of Advanced Robotic Systems- world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career, since it was a pathway to founding IntechOpen - Open Access publisher focused on addressing academic researchers needs. Alex is a personification of IntechOpen key values being trusted, open and entrepreneurial. Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. He is an expert in structural, absorptive, catalytic and photocatalytic properties, in structural organization and dynamic features of ionic liquids, in magnetic interactions between paramagnetic centers. The author or co-author of 3 books, over 200 articles and reviews in scientific journals and books. He is an actual member of the International EPR/ESR Society, European Society on Quantum Solar Energy Conversion, Moscow House of Scientists, of the Board of Moscow Physical Society.",institutionString:null,institution:{name:"Semenov Institute of Chemical Physics",country:{name:"Russia"}}},{id:"62389",title:"PhD.",name:"Ali Demir",middleName:null,surname:"Sezer",slug:"ali-demir-sezer",fullName:"Ali Demir Sezer",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62389/images/3413_n.jpg",biography:"Dr. Ali Demir Sezer has a Ph.D. from Pharmaceutical Biotechnology at the Faculty of Pharmacy, University of Marmara (Turkey). He is the member of many Pharmaceutical Associations and acts as a reviewer of scientific journals and European projects under different research areas such as: drug delivery systems, nanotechnology and pharmaceutical biotechnology. Dr. Sezer is the author of many scientific publications in peer-reviewed journals and poster communications. Focus of his research activity is drug delivery, physico-chemical characterization and biological evaluation of biopolymers micro and nanoparticles as modified drug delivery system, and colloidal drug carriers (liposomes, nanoparticles etc.).",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"61051",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"100762",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"St David's Medical Center",country:{name:"United States of America"}}},{id:"107416",title:"Dr.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Texas Cardiac Arrhythmia",country:{name:"United States of America"}}},{id:"64434",title:"Dr.",name:"Angkoon",middleName:null,surname:"Phinyomark",slug:"angkoon-phinyomark",fullName:"Angkoon Phinyomark",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/64434/images/2619_n.jpg",biography:"My name is Angkoon Phinyomark. I received a B.Eng. degree in Computer Engineering with First Class Honors in 2008 from Prince of Songkla University, Songkhla, Thailand, where I received a Ph.D. degree in Electrical Engineering. My research interests are primarily in the area of biomedical signal processing and classification notably EMG (electromyography signal), EOG (electrooculography signal), and EEG (electroencephalography signal), image analysis notably breast cancer analysis and optical coherence tomography, and rehabilitation engineering. I became a student member of IEEE in 2008. During October 2011-March 2012, I had worked at School of Computer Science and Electronic Engineering, University of Essex, Colchester, Essex, United Kingdom. In addition, during a B.Eng. I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). 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