Epidemiological criteria for assessing IDD in a population based on median urinary iodine concentration.
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Dr. Tiefenbacher has published more than 200 papers on a diverse array of topics that examine perception and behaviors with regards to the application of pesticides, releases of toxic chemicals, environments of the U.S.-Mexico borderlands, wildlife hazards, and the geography of wine.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"73876",title:"Dr.",name:"John P.",middleName:null,surname:"Tiefenbacher",slug:"john-p.-tiefenbacher",fullName:"John P. Tiefenbacher",profilePictureURL:"https://mts.intechopen.com/storage/users/73876/images/system/73876.jfif",biography:"Dr. John P. Tiefenbacher (Ph.D., Rutgers, 1992) is a professor of Geography at Texas State University. His research has focused on various aspects of hazards and environmental management. Dr. Tiefenbacher has published on a diverse array of topics that examine perception and behaviors with regards to the application of pesticides, releases of toxic chemicals, environments of the U.S.-Mexico borderlands, wildlife hazards, and the geography of wine. More recently his work pertains to spatial adaptation to climate change, spatial responses in wine growing regions to climate change, the geographies of viticulture and wine, artificial intelligence and machine learning to predict patterns of natural processes and hazards, historical ethnic enclaves in American cities and regions, and environmental adaptations of 19th century European immigrants to North America's landscapes.",institutionString:"Texas State University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"6",institution:{name:"Texas State University",institutionURL:null,country:{name:"United States of America"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"12",title:"Environmental Sciences",slug:"environmental-sciences"}],chapters:[{id:"76073",title:"Integrating Ecological Site Descriptions with Soil Morphology to Optimize Forest Management: Three Missouri Case Studies",slug:"integrating-ecological-site-descriptions-with-soil-morphology-to-optimize-forest-management-three-mi",totalDownloads:20,totalCrossrefCites:0,authors:[{id:"185895",title:"Dr.",name:"Michael",surname:"Aide",slug:"michael-aide",fullName:"Michael Aide"},{id:"269286",title:"Dr.",name:"Christine",surname:"Aide",slug:"christine-aide",fullName:"Christine Aide"},{id:"269287",title:"Dr.",name:"Indi",surname:"Braden",slug:"indi-braden",fullName:"Indi Braden"}]}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"194667",firstName:"Marijana",lastName:"Francetic",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/194667/images/4752_n.jpg",email:"marijana@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"66237",title:"Urinary Iodine: Biomarker for Population Iodine Nutrition",doi:"10.5772/intechopen.84969",slug:"urinary-iodine-biomarker-for-population-iodine-nutrition",body:'All iodine in the blood is in the iodide form either it is taken up by the thyroid and converted into thyroid hormone or being excreted in the urine. Almost 90% of the ingested iodine is excreted in the urine. Therefore, urinary iodine excretion is a good biomarker of very recent dietary iodine intake [1]. On an individual basis, 24-hour urine sample is necessary for the assessment of iodine intake as the level is more consistent in iodine-deficient populations than in those with adequate iodine intake (Figure 1). On a population basis, the median urinary iodine concentration (mUIC) of spot urine from sufficiently large randomly selected 8–10-year-old children or adults has been shown to provide useful information on the average iodine intake or status of a community. On an individual basis, urinary iodine varies from day to day and even within a given day. However, this variation tends to even out among population [2]. Most of the epidemiological IDD studies had emphasised on rapid inexpensive methods of urinary iodine determination that could be applied to a large number of samples [3].
Degrees of iodine intake (iodine nutrition status) and their suitable types of human sample collection to determine the median urinary iodine concentration (mUIC).
The main biochemical indicator that is widely used for the assessment of IDD is urinary iodine concentration (mUIC) [4]. The advantages of mUIC as an indicator of IDD are that the method directly reflects iodine supply of the individual, it is objective and non-invasive and urine samples can be kept for later analysis. However, the disadvantages of this method are that it requires laboratory space, special facilities and skilled technician to provide accurate determinations. In addition, this method reflects only current but not past intake of iodine [5].
Epidemiological studies stated that the population distribution of urinary iodine is required rather than individual levels. The frequency distribution of urinary iodine usually skewed towards elevated values; hence, the median value is considered instead of the mean as indicating the status of iodine nutrition [1]. The mUIC of 100 μg/L and above defines a population which has no IDD; i.e. at least 50% of the sample should be >100 ug/L. In addition, not more than 20% of sample should be below 50 μg/L. Iodine nutrition status is based on six categories of urinary excretion classification (Table 1) [3].
Median urinary iodine concentration (μg/L) | Severity of IDD |
---|---|
<20 | Severe deficient |
20–49 | Moderate deficient |
50–99 | Mild deficient |
100–199 | Optimal |
200–299 | More than adequate |
>300 | Excessive |
Epidemiological criteria for assessing IDD in a population based on median urinary iodine concentration.
Source: Ref. [3].
Iodine is grouped under micronutrients, and it is needed in small amount, but it is very important for the development of optimum human growth. Iodine is needed in the synthesis of thyroid hormones [6]. Through iodination, one, two, three or four iodine atoms are bound to tyrosine to form monoiodothyronine (MIT), diiodothyronine (DIT), triiodothyronine (T3) or thyroxine (T4), respectively, through the action of iodinase enzyme. Iodine is absorbed from the gastrointestinal system, will enter the blood circulation and will be transported into the thyroid follicle cells through the sodium/iodine (Na/I) symporter. In iodide form, it will then be transported to the thyroid follicle colloid through pendrin. Concurrently, thyroglobulin (TG) is being synthesised in the endoplasmic reticulum (ER) and being secreted into the follicle colloid through exocytosis. TG is the transporter protein of the thyroid hormones in the thyroid follicle colloid. It consists of branches of tyrosine molecules which will then be bound to iodine through the iodination process, forming the MIT and the DIT. When one MIT and one DIT bind, T3 will be formed, while upon binding of two DITs, T4 will then be formed. These TG-bound thyroid hormones will enter the thyroid follicular cell through endocytosis. TG will then undergo proteolysis, and T3 and T4 will be transported into the blood circulation through the MCT symporter [7] (Figure 2).
Thyroid hormone synthesis in the thyroid gland (image reproduced with permission from the rights holder, Journal of Thyroid Research) [
Iodine is a micronutrient which is present in the body in minute amount. The quantity of iodine required by an individual is about 150–200 μg/day [8]. Its main role is in the synthesis of thyroid hormone which is essential for the brain and physical development [9]. The regulation of thyroid hormones is under the control of the pituitary gland through thyroid-stimulating hormone (TSH). TSH secretion is regulated by a ‘feedback’ mechanism related to the level of thyroid hormones thyroxine [3,5,3′,5′-tetraiodothyronine (T4)] in the blood. Iodine is needed in the human body, and as the blood T4 falls, the pituitary TSH secretion is increased. In severe iodine deficiency disorders (IDD), the level of T4 remains lowered, and the level of TSH remains elevated. Both these measurements are used for diagnosis of hypothyroidism due to IDD at various stages in life particularly in neonates [10].
Most of the iodine exists in the ocean and seafood, including saltwater fish, shellfish, kelp, seaweed and seaweed products which can provide a considerable amount of iodine [11]. Iodine exists in the sea and the soil as iodide. Iodide ions are oxidised by sunlight to elemental iodine which is volatile. The iodine cycle in nature is complete if the concentration of iodide in the seawater is about 50–60 μg/L, approximately 0.7 μg/m3 in the air, and the iodine in the atmosphere is returned to the soil through rain, with concentrations in the range of 1.8–8.5 μg/L. Iodine deficiency occurs in the soil when the return of the iodine to the soil is slow and in small amount compared to the original loss of iodine. Hence, all crops grown in this soil will be iodine deficient [12]. Low levels of iodine in the diet for people who do not get enough iodine from their food may lead to health problems collectively referred to as iodine deficiency disorders (IDD) [14].
IDD is a major public health problem for population throughout the world which affects human from early foetal life through to adulthood [15]. Although IDD can affect any person of any age, pregnant women and children are the most vulnerable high-risk group for IDD [16]. Iodine requirement is high during pregnancy; it may increase by 50% because of increased maternal thyroxine production [14].
IDD in the foetus is the result of IDD in the mother, and this condition is associated with greater incidence of stillbirths, abortions, congenital abnormalities, neurological cretinism and psychomotor defects (Figure 3). In neonate, apart from mortality, the continuing severe IDD may affect the brain and physical development. Low birth weight is normally associated with a higher rate of congenital anomalies, and there were also evidences on substantial fall in infant mortality with improved birth weight following the iodized oil injection. IDD in the child and adolescent is associated with juvenile hypothyroidism, impaired mental function and retarded physical development. Studies on schoolchildren living in iodine-deficient areas indicated impaired school performance and IQs [17], while IDD in the adult had effects on their individual capacity, initiative and decision-making (Figure 3). These results indicate that IDD can be a major obstacle to human and social development of population living in an iodine-deficient environment. Therefore, correction of iodine deficiency is considered as a major contribution to population development [18].
Effect of iodine deficiency and the spectrum of IDD across the life span (clinical presentation) in various age groups, i.e. foetus, neonate, infant, child, adolescent and adult.
Pregnant woman is one of the most susceptible groups for iodine deficiency. An adequate intake of iodine in the diet of pregnant woman is important to ensure normal growth and development of the foetus. During pregnancy, iodine requirement increases substantially to ensure adequate supply to the foetus particularly for healthy brain development. Iodine deficiency during pregnancy can cause maternal and foetal hypothyroidism and impairs neurological development of the foetus since it is secondary to transplacental passage of iodide. The consequences depend upon the timing and severity of hypothyroidism; the most severe manifestation is cretinism [14].
Since most foods have relatively low iodine content, Universal Salt Iodization (USI) programmes are executed. However, in countries or setting where USI is not possible, other mode of iodine supplementation needs to be implemented. It is difficult to accurately quantify iodine intakes using traditional methods of dietary assessment in terms of the contribution of iodized salt use from table and cooking to total iodine intake. In view of the limitations of dietary assessment for adequate iodine, a mUIC of 150–249 μg/L has been established to determine the adequate iodine status among pregnant women. However, the large intra-individual variation in UIC from either spot or 24-hour urine samples means that UIC cannot be used to assess iodine status in an individual pregnant woman. Therefore, the association between iodine status in pregnancy and the developmental outcome of the individual child is rather difficult to be assessed.
Universal Salt Iodization (USI) is currently the most widely used strategy towards sustainable control and elimination of IDD. There was a significant progress since the adoption of USI as a primary strategy to address IDD in 1993. Iodizing table salt is one of the best and least expensive methods of preventing IDD. Salt is used as a key vehicle as it is widely available and consumed in a regular amount throughout the year apart from a very low cost of salt iodization with US$ 0.05 per person per year [1]. This strategy has been implemented in most countries where iodine deficiency is a public health problem.
Various concerted global efforts have also been undertaken to eliminate IDD. This includes extensive advocacy from the international partners/alliances such as the WHO, UNICEF and ICCIDD (International Council for Control of Iodine Deficiency Disorders). These alliances have been in the forefront in helping countries to set up national salt iodization programmes. As reported by WHO/UNCEF/ICCIDD, there are currently 65 countries worldwide implementing USI as an effective strategy to eliminate IDD [3]. However, an effective USI in correcting iodine deficiency adequately through iodized salt must reach the whole affected population including pregnant women and children. Therefore, close and regular monitoring of iodized salt at various levels from the production, importation, retailer and household is crucial. Such monitoring requires close collaboration between the governments, salt industries and importers. In countries or areas within countries where USI is not possible, iodine supplementation needs to be implemented and especially targeted to pregnant women and children until USI is scaled up.
Upon consumption, the needed amount of iodine is retained in the body, while excess iodine is excreted. Thus, high urinary iodine concentration does not reflect a disease state yet, but if persists on repeated urine sample, further blood tests is recommended. Urinary iodine reflects the food consumption taken overnight, and it is just an immediate biomarker (short-term reflection) for iodine intake. Thus, the long-term reflection of iodine intake will be more representative by measuring blood thyroglobulin (TG) as it is synthesised parallel to the amount of iodine present in the thyroid follicular cells. The very low or high individual urinary iodine readings will usually be repeated for testing to ensure that it is replicating the first reading.
For respondents with high mUIC, other biomarkers such as blood thyroglobulin (TG), thyroid-stimulating hormone (TSH), thyroid hormones (free thyroxine, fT4; free triiodothyronine, fT3) and thyroid antibodies, thyroid peroxidase antibodies (TPO Ab) and thyroglobulin antibodies (TgAb) are thus suggested for further diagnosis. Brief information on these biomarkers is as stated below:
T4 is a molecule of thyronine bond to four atoms of iodine, while T3 has three iodine atoms. T4 is more abundant than T3, but through deiodinase activity, the more potent T3 is synthesised. Low level of T4 usually indicates hypothyroidism. For clinical biochemistry free T4 (fT4) and free T3 (fT3) are usually measured as these are the biologically active forms. Reference intervals for fT4 and fT3 are as stated in Table 2.
Whole group (n = 870) | Constraint group (n = 453) | |||||
---|---|---|---|---|---|---|
Hormone | Median | Minimum-Maximum | 2.5th–97.5th percentilesa | Median | Minimum-Maximum | 2.5th–97.5th percentilesa |
TSH, mIU/L | 1.31 | 0.05–14.50 | 0.30–3.63 | 1.36 | 0.12–5.29 | 0.40–3.77b |
T4, nmol/L | 101.00 | 52.10–209.00 | 71.50–158.00 | 98.30 | 61.80–173.00 | 70.50–157.00 |
T3, nmol/L | 1.77 | 0.89–4.00 | 1.23–2.80 | 1.77 | 0.89–3.96 | 1.27–2.79 |
FT4, pmol/L | 16.20 | 8.24–28.60 | 12.70–20.80 | 16.20 | 9.30–24.70 | 12.80–20.40 |
FT3, pmol/L | 5.10 | 2.52–9.96 | 3.89–6.66 | 5.13 | 2.52–9.96 | 4.02–6.79 |
Reference intervals for thyroid hormones from subjects with normal thyroid gland assessed sonographically (table reproduced with permission of the rights holder, Clinical Chemistry) [19].
Data are reported as empirical percentiles.
The lower limit of the TSH reference interval in the constraint group was >5% different from the comparable limit of the whole group.
TSH is released upon the induction by thyrotropin-releasing hormone (TRH), secreted from the hypothalamus. TRH is secreted when serum T3 and/or T4 is low. TSH induces the production of thyroid hormones T3 and T4. Low level of TSH usually indicates hyperthyroidism (parallel to high levels of T3 and/or T4) [17]. Reference interval for TSH is as stated in Table 2.
TG is the globulin where binding of iodine to tyrosine to form thyroid hormones takes place. It is the long-term biomarker for iodine status in a human, besides urinary iodine as the short-term biomarker for iodine nutrition.
The median for reference interval for dried blood spot (DBS) TG from 5- to 14-year-old children before intervention of iodized salt is 49 g/L. After using iodized salt for 5 months, the DBS-TG decreased to 13 g/L and further decreases to 8 g/L after 10 months of consumption of iodized salt [20].
This antibody is for binding to the antigen thyroid peroxidase (TPO) enzyme which is responsible for thyroid hormones synthesis. Once the enzyme is bound to the antibody, less free unbound enzymes are available for thyroid hormone synthesis, thus causing lower thyroid hormone production. TgAb is the antibody for the globulin TG. With the presence of elevated amount of TgAb, the thyroglobulin (TG) will bind to its antibody, and lesser TG is available to bind to the thyroid hormones for transportation in the blood vessels, thus causing lesser thyroid hormones being circulated in the human body [21]. The reference intervals are 15 kIU/L for TPOAb and 31 kIU/L for TgAb [22] (Figure 4).
Subsequent biomarker testing and further action for individual and population urinary iodine estimation.
Both insufficient and excessive iodine intake can result in thyroid dysfunctional diseases. If the thyroid diseases are due to iodine-induced phenomena, the main management is to avoid or reduce iodine intake, followed by the appropriate drugs if symptomatic or there is abnormality with the thyroid function test (TFT) results.
Iodine-induced hypothyroidism can occur in normal individuals and in those with chronic systemic disease and underlying thyroid disorders. It has been seen in patients who had a history of post-partum thyroiditis and subacute thyroiditis and in those treated with recombinant interferon-alpha. The hypothyroidism was described as transient, and thyroid function returns to normal in 2–3 weeks after iodide withdrawal. Some patients may require transient T4 replacement therapy [23].
The presenting clinical features of hypothyroidism depend on the duration and severity, the nature of its onset and the patient’s psychological characteristics [24]. The following are the signs and symptoms of hypothyroidism:
Fatigue
Weight gain from fluid retention
Dry skin and cold intolerance
Yellow skin
Coarseness or loss of hair
Hoarseness
Goitre
Reflex delay, relaxation phase
Ataxia
Constipation
Memory and mental impairment
Decreased concentration
Depression
Irregular or heavy menses and infertility
Myalgias
Hyperlipidaemia
Bradycardia and hypothermia
Myxoedema fluid infiltration of tissues
When there is clinical suspicion of hypothyroidism, a thyroid function test should be performed. Measurement of TSH level is the primary test to confirm primary hypothyroidism. Other laboratory evaluation may include free T4 and thyroid antibodies (anti-thyroid peroxidase and anti-thyroglobulin autoantibodies). Imaging studies to evaluate any structural thyroid abnormalities include a thyroid scan, ultrasonography or both [24]. When iodine deficiency occurs during pregnancy, it is associated with foetal hypothyroidism, mental impairment and increased neonatal and infant mortality [25]. In adults, iodine-induced hypothyroidism is rare. The most common manifestation is goitre. Low iodine intake leads to reduced T4 and T3 production which results in increased TSH secretion in an attempt to restore normal T4 and T3 production. TSH also stimulates thyroid growth leading to goitre. The goitre is initially diffuse but progresses to nodular goitre and eventually to thyroid autonomy and possible hyperthyroidism [26]. Excess iodine ingestion or exposure above the limit of the recommended daily iodine intake induces thyroid dysfunction. Iodine-induced thyroid dysfunction may be subclinical or overt. Excess iodine is generally well tolerated. However, individuals with underlying thyroid disease or other risk factors may be susceptible to iodine-induced thyroid dysfunction following acute or chronic exposure.
Individuals with underlying thyroid disease:
Euthyroid Graves’ disease previously treated by radioactive iodine, thyroidectomy or anti-thyroid drugs
Hashimoto’s thyroiditis
Euthyroid with a history of subacute thyroiditis
Euthyroid with a history of post-partum thyroiditis
Euthyroid with a history of type 2 amiodarone-induced thyrotoxicosis
Euthyroid posthemithyroidectomy
Euthyroid after interferon-alpha therapy
The spectrum of iodine deficiency disorders (IDD) is seen across the life span in various age groups, i.e. foetus, neonate, infants, child, adolescent and adult. They include endemic goitre and cretinism, endemic mental retardation, decreased fertility rate, increased perinatal death and infant mortality and varying degrees of other growth and developmental abnormalities (Table 3) [27, 28]. Hypothyroidism due to very low iodine intake is now extremely rare. Adults usually have the typical clinical manifestations of hypothyroidism and goitres [29].
Life stage | Spectrum of IDD |
---|---|
Foetus | Abortions Deaf mutism Stillbirths Congenital anomalies Increased perinatal mortality Endemic cretinism |
Neonate | Neonatal goitre Neonatal hypothyroidism Endemic mental retardation Increased susceptibility of the thyroid gland to nuclear radiation |
Child and adolescent | Goitre Subclinical hypothyroidism Impaired mental retardation Retarded physical development Increased susceptibility of the thyroid gland to nuclear radiation |
Adult | Goitre with its complications Hypothyroidism Impaired mental function Hyperthyroidism in the elderly (after iodized salt) |
Iodine-induced hyperthyroidism can occur after intake of excess iodine in the diet, exposure to radiographic contrast media for imaging procedures or medications [30]. In iodine-sufficient areas, iodine can induce hyperthyroidism in euthyroid patients with previous thyroid diseases. These include patients who were treated with anti-thyroid drugs for Grave’s disease and post-partum thyroiditis [31, 32].
The severity and spectrum of symptoms and signs of hyperthyroidism may be related to the duration of the illness, the effects of excess thyroid hormone and the age of the patient [24].
The symptoms and signs include the following:
Nervousness and irritability
Palpitations and tachycardia
Heat intolerance or increased sweating
Tremor
Weight loss or gain
Alterations in appetite
Frequent bowel movements or diarrhoea
Dependent lower-extremity oedema
Sudden paralysis
Exertional intolerance and dyspnoea
Menstrual disturbance (decrease flow)
Impaired fertility
Mental disturbances
Sleep disturbances (including insomnia)
Changes in vision, photophobia, eye irritation, diplopia or exophthalmos
Fatigue and muscle weakness
Goitre (depending on cause)
Pretibial myxoedema
In the Iodine Global Network newsletter published on its website, Prof. Dr. Zimmermann had laid out the strategies needed for the vulnerable groups, i.e., the newborns, infants and the children. He had suggested that these tests should be done on these groups respectively: blood thyroid-stimulating hormone, urinary iodine and blood spot thyroglobulin (http://www.ign.org/zimmermann-calls-for-new-strategies-against-idd.htm). He also suggested using the TSH measurement in the newborn screening for iodine assessment. Commonly, iodine-deficient newborns present with elevated TSH. The WHO reported that if the TSH level is greater than 5 mIU/L from the whole blood of 3% of the newborns measured after 3–4 days post-birth, this would indicate that the population is iodine deficient. Another suggestion made by him was to use the newborns’ urinary iodine as a marker of IDD in addition to the current practise of measuring the median urinary iodine of the schoolchildren. Using a non-invasive system, urine was collected from infants, and study had shown that in 1200 infants, the baseline TSH of 77 μg/L had increased to 100 μg/L after 4 days post-birth. In addition to that, a system for collecting young children blood spot was done to measure their TG concentration, and a reference range of 4–40 μg/L had been determined. Noteworthy, there are challenges in order to establish a specific international reference range among newborns as there will be differences between the population from the USI areas and the non-USI areas.
Excess urinary iodine is generally well tolerated, but individuals with underlying thyroid disease or other risk factors may be susceptible to iodine-induced thyroid dysfunction following acute or chronic exposure. Increased iodine exposure including the global public health efforts of iodine supplementation, the escalating use of iodinated contrast radiologic studies, amiodarone administration in vulnerable patients, excess seaweed consumption and various miscellaneous sources should be looked for.
Iodine-induced thyroid dysfunction may be subclinical or overt. Recognition of the association between iodine excess and iodine-induced hypothyroidism or hyperthyroidism is important in the differential diagnosis of patients who present without a known cause of thyroid dysfunction.
It is declared that there is no conflict of interest involved in the publication of this book chapter.
Plant-derived drugs have been part of the human race in the healthcare for thousands of years [1]. Throughout the world, a huge percentage of population depends upon the use of plant-based medicine because of their easy availability and also due to the lack of better healthcare alternatives. Plant-based medicines or herbal medicines have been effective and safe traditional methods practiced in many countries including China, India, and most African countries for the treatment of various diseases [2]. A large number of plant extracts, concoctions, poultices, decoctions, or pastes are equally used in many countries for treatment of diseases, cuts, wounds, and burns. Thus, since antiquity, several medicinal plants and plant-based strategies are widely known for their significant role in wound healing and skin regeneration as well as their therapeutic applications [2].
\nWound is an injury that damages the dermal layer of the skin. Several factors contribute to wound generation, e.g., accidental traumas or surgery, and in certain cases, this dermal injury may have a devastating outcome [2, 3]. Wound healing is the natural process which leads to restore the structural and functional integrities of injured tissues. It involves several biochemical and cellular pathways, in order to repair the lesions and to restore the physiological conditions. Fortunately, the human body has the inbuilt capacity to promote this repairing process. However, there can be impairment of this sophisticated repairing process leading to chronic or non-healing wounds, which may result in severe clinical complications or even patient death. Deficiencies in nutritional factors which are essential in cellular differentiation, immune functioning, and collagen formation may result to the failure of wound healing process [4]. Additionally, oxygen- and nitrogen-centered reactive species are known to play crucial roles in regulating healing [2, 5]. Hence, high concentrations of these reactive species are present in wound sites. Unfortunately, these substances can induce harmful effects on cells and tissues and even promote oxidative stress that generates lipid peroxidation, damage of deoxyribonucleic acid (DNA), and enzyme inactivation, including free radical scavenger enzymes [6]. This necessitates the involvement or use of antioxidants which may represent potential therapeutic tools to enhance and accelerate wound healing process.
\nSeveral phytoconstituents such as triterpenes, alkaloids, and polyphenols show antioxidant and antimicrobial effects and are able to promote one or more mechanisms of the reparative process [7]. Accordingly, numerous plant extracts have been employed to promote wound healing with a high degree of success [8]. Many wound healing medicinal plants have been investigated to possess antioxidant properties. In other dimensions, numerous studies conducted over the years showed the great potential of plants in promoting wound healing, by virtue of their high contents in antioxidant properties. This document therefore intends to throw more light on the existing literature on wound healing potentials of medicinal plants and their antioxidant properties.
\nA physical, chemical, thermal, microbial, or immunological action on the living tissue may result in disruption of a cellular, anatomical, and functional continuity of the living tissue [9]. This phenomenon results in an injury to the skin or the underlying tissue or organ termed a wound. A wound is therefore damage or disruption to the normal anatomical structure and function [10, 11]. This can range from a simple break in the epithelial integrity of the skin or it can be deeper, extending into subcutaneous tissue with damage to other structures such as tendons, muscles, vessels, nerves, parenchymal organs, and bones [12, 13].
\nWound can result through accident or intentional etiology or as a result of a disease process. Wounding, irrespective of the cause and whatever the form, damages the tissue and disrupts the local environment within it [14].
\nBased on the underlying cause of wound creation, wounds may be classified into two main groups: open and closed wounds. In open wounds, the skin is broken, and the underlying tissue is exposed to the outside environment allowing blood to leave the body. These are wounds in which there is loss of superficial surface covering the tissue such as loss of skin. Such wounds are opened to invasion by microorganisms [15]. Open wounds consist of abrasion or glazes, laceration, incision, puncture, avulsion, cuts, blisters, penetration, and gunshot wounds. In closed wounds, the skin is intact, and the underlying tissue is not directly exposed to the outside world. The superficial surface covering the wound is not lost. The wound occurs under the surface of the skin without affecting the skin and hence does not involve any external bleeding. Infection of these wounds is rare, and it may resolve without any treatment if it is not extensive. Examples of closed wounds are contusion (bruises), hematomas, and crush injuries.
\nWound can also be classified as either internal or external based on the wound origin. Internal wounds result from impaired immune and nervous system functions and/or decreased supply of blood, oxygen, or nutrients to that area, such as in cases of chronic medical illness (diabetes, atherosclerosis, and deep vein thrombosis). External wounds are usually caused by penetrating objects or non-penetrating trauma. Penetrating wounds result from trauma that breaks through the full thickness of the skin, reaching down to the underlying tissue and organs, and include stab wounds (trauma from sharp objects, such as knives), skin cuts, surgical wounds (intentional cuts in the skin to perform surgical procedures), and gunshot wounds (wounds resulting from firearms).
\nNon-penetrating wounds are usually the result of blunt trauma or friction with other surfaces; the wound does not break through the skin and may include abrasions (scraping of the outer skin layer), lacerations (a tear-like wound), contusions (swollen bruises due to accumulation of blood and dead cells under the skin), and concussions (damage to the underlying organs and tissue on the head with no significant external wound).
\nDepending on the healing time, wound can further be classified as either acute or chronic wounds [14]. Acute wounds heal uneventfully (with no complications) in the predicted amount of time, while chronic wounds take a longer time to heal and might have some complications.
\nThe presence of foreign material and bacteria leads to another way to classify wounds. A wound that has dirt, fragments of the causative agent, bacteria, or other foreign materials is determined to be contaminated or infected. A wound with no foreign materials or debris inside is determined to be clean [15].
\nWound healing is a complex and dynamic process of replacing devitalized and missing cellular structures and tissue layers. The wound healing process can be divided into three or four distinct basic phases. Inflammatory, fibroblastic or proliferation, and maturation or remodeling constitutes the three-phase division [16, 17]. In the four-phase concept, there are the hemostasis phase, the inflammatory phase, the proliferation phase, and the remodeling phase. In the three-phase approach, the hemostasis phase is contained within the inflammatory phase [18]. The normal physiology of wound healing depends on low levels of reactive oxygen species (ROS) and oxidative stress [19, 20]. An overexposure to oxidative stress leads to impaired wound healing. Free radicals are highly unstable molecules, and ROS are a form of free radicals that include the oxygen atom as well as reactive molecules such as superoxides and peroxides. Although normally formed as a by-product of metabolism and are reactive to invading organisms, overproduction leads to an increased load of free radicals and ROS known as oxidative stress. Free radicals attack and remove electrons from all types of molecules in the cell, including nucleic acids in DNA, proteins, and polyunsaturated fatty acids in cell membranes or organelle membranes. When free radicals attack proteins, they break peptide bonds in the protein backbone, changing the protein structure and altering its functionality [21]. All of these processes are detrimental to the proliferation of new cells in the healing process of epithelial wounds. ROS are likely needed at some basal level for wound healing. The importance of ROS to wound healing is illustrated by studies demonstrating that total suppression of oxidant production results in impaired healing, just as excessive amounts of oxidants do. ROS have also been implicated as important mediators of cell signaling and inflammation in wound repair. Although ROS production is physiologic, excessive production can be harmful.
\nOxidation is a basic part of the aerobic life and our metabolism. The body uses oxygen (O2) to produce energy by oxidizing glucose. In the biochemical process involving oxygen, i.e., during oxidation, many highly unstable reactive molecules called free radicals are produced. The free radicals are atoms or molecules having odd number of electrons. Atoms of oxygen or nitrogen having central unpaired electron are called reactive oxygen or nitrogen species [22, 23]. These species are natural by-products produced by the normal metabolism of oxygen in living organisms. These reactive oxygen species (ROS) are various forms of activated oxygen which causes oxidative damage. They include free radicals such as superoxide anion radicals (O2)−, hydroxyl radicals (OH˙), and non-free radical species such as peroxyl radicals (O2)−2 and singlet oxygen (1O2) which are various forms of activated oxygen generated in the body [24].
\nIn small amounts, these ROS can be beneficial as signal transducers and growth regulators. However, during oxidative stress, large or excessive amounts of these ROS can be produced and may be dangerous and harmful to the body. The free radicals have the potential to damage biological tissues by disrupting cell membranes. This then affects the ability of the cell to transport substances across the membranes. The immune system is vulnerable to oxidative stress. Oxidative stress refers to an imbalance between the production of free radicals and the antioxidant defense system. It is the accumulated damage due to free radical activity in the human body. Excessive amounts of ROS may be a primary cause of biomolecular oxidation. The ROS have the ability to attack numerous molecules in the membrane that contain carbon–carbon double bonds (C〓C). For instance, polyunsaturated fatty acids are particularly sensitive to free radicals. The free radicals are destructive to these molecules including proteins and lipids through oxidation [25]. As a result, ROS have the potential of causing peroxidation of membrane lipids, aggression of tissue membranes and proteins, or damage to DNA and enzyme and generally by oxidizing low-density lipoproteins (LDL). This may result in significant damage to cell structure, contributing to various diseases, such as cancer, stroke, diabetes, arthritis, hemorrhagic shock, coronary artery diseases, cataract, cancer, and acquired immune deficiency syndrome (AIDS) as well as age-related degenerative brain diseases [26]. Under normal circumstances, the cell can reduce the impact of these free radicals and ROS by an endogenous system, i.e., by the body’s natural antioxidant defense mechanisms. Physiologic antioxidant defenses include the ROS-detoxifying enzymes superoxide dismutase (SOD), catalase, glutathione peroxidases, and peroxiredoxins [27]. However, the following factors or conditions may contribute to the overproduction of ROS and antioxidant depletion: the mitochondrial electron transport chain; excessive stimulation of nicotinamide adenine dinucleotide phosphate (NADPH); exposure to environmental pollutants such as cigarette smoke, ultraviolet (UV) rays, radiation and toxic chemicals which weaken the body’s defense system; and exposure to explosion-generated shock waves [28, 29]. It becomes evidently clear that the devastating impact of ROS can only be reduced successfully through exogenous systems. There is therefore the need to provide the body with a constant supply of antioxidants through dietary supplementation. Antioxidants are postulated to help control wound oxidative stress and thereby accelerate wound healing. They are important mediators in regulating the damage that is potentially incurred by biological molecules such as DNA, protein, lipids, and body tissue in the presence of reactive species.
\nAntioxidants are substances that prevent oxidation to occur. They are compounds that detoxify ROS to prevent their damaging effects through multi-mechanisms. Antioxidants may offer resistance against the oxidative stress by scavenging free radicals, inhibiting lipid peroxidation and thus preventing disease. Antioxidants have the ability to prevent, delay, or ameliorate many of the effects of free radicals. During certain diseased state, as well as during aging, there is a need to boost the antioxidant abilities, thereby potentiating the immune mechanism [30]. The antioxidants preserve and stimulate the function of immune cells against homeostatic disturbances [31].
\nSynthetic antioxidants such as butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), and tertiary butylhydroquinone (TBHQ) are commonly employed as preservatives or additives by pharmaceutical, cosmetic, and food companies [32]. The free radicals are known to be scavenged by these synthetic antioxidants. However, reports on the involvement of synthetic antioxidants in chronic diseases and their adverse side effects leading to carcinogenicity have restricted their use in foods. Therefore, attention has been focused on natural antioxidants mainly from plant sources [33, 34].
\nThere is great interest in the use of natural products, which include compounds derived from fruits, plants, and herbs. Plants have an innate ability to synthesize a wide variety of phytochemicals. Plants do not only provide the carbohydrates, proteins, and fats necessary in the diet of man and other animals but also produce a vast range of organic materials to perform their normal physiological functions and to protect themselves from microbial pathogens and animal herbivores and to respond to environmental stress conditions. Hence plants accumulate a range of low- and high-molecular weight secondary metabolites that play important roles in ROS metabolism and avoidance of uncontrolled oxidation of essential biomolecules.
\nConsequently, plants have efficient complex enzymatic and non-enzymatic antioxidant defense systems to avoid the toxic effects of free radicals. Enzymatic systems include SOD, catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), while non-enzymatic systems consist of low-molecular weight antioxidants (ascorbic acid, glutathione, proline, carotenoids, phenolic acids, flavonoids, etc.) and high-molecular weight secondary metabolites such as tannins [35, 36]. Figure 1 gives a summary of the different classifications of antioxidants.
\nFlow chart showing the different classifications of antioxidants.
Among all secondary metabolites, phenolic compounds have been mentioned to be largely the contributory compound to antioxidant activity of plants since they have shown promising antioxidant activity in many in vivo and in vitro studies. Phenolic compounds exhibit a considerable free radical scavenging (antioxidant) activity, which is determined by their reactivity as hydrogen or electron-donating agents, the stability of the resulting antioxidant-derived radical, their reactivity with other antioxidants, and finally their metal-chelating properties [37, 38]. Similarly, polyphenols derived from plants are of great importance because of their potential antioxidant and antimicrobial properties [39]. Plant phenolics are mainly classified into five major groups as phenolic acids, flavonoids, lignans, stilbenes, and tannins. These classes of phytochemicals are found to have excellent antioxidant activity and are widely available for the treatment of a multitude of cutaneous ailments. Many studies have presented plants to possess great potential for wound healing because they are versatile as antioxidant and antimicrobial sources. Medicinal plants and their active compounds have been used in medicine since ancient times and are well known for their abilities to promote wound healing and prevent infection without grave side effects [40].
\nFlavonoids are a group of polyphenolic compounds with known properties which include free radical scavenging, inhibition of hydrolytic and oxidative enzymes, and anti-inflammatory action [41]. The best-described property of almost every group of flavonoids is their capacity to act as antioxidants. The flavones and catechins seem to be the most powerful flavonoids for protecting the body against reactive oxygen species. Flavonoids may have an additive effect to the endogenous scavenging compounds. Many in vitro studies have demonstrated the potent peroxyl radical scavenging abilities of flavonoids, which contribute to inhibiting lipid peroxidation and oxidation of LDL [42].
\nFlavonoids are known to possess protective effects in biological systems due to their capacity to transfer free radical electrons, chelate metal catalysts, activate antioxidant enzymes, reduce alpha-tocopherol radicals, and inhibit oxidases [43]. Flavonoids have lower redox potentials hence are able to reduce highly oxidizing free radicals by forming less reactive flavonoid radicals. As a result, they are able to prevent lipid peroxidation which is one of the most important actions of free radicals that leads to cellular membrane damage and, ultimately, to cell death [44]. Flavonoids are also able to scavenge nitric oxide which forms in combination with superoxide free radicals the highly damaging peroxynitrite and also to inhibit xanthine oxidase, an important biological source of superoxide radicals that can react with hydrogen peroxide to produce a more toxic hydroxyl radical [44].
\nOther flavonoids such as quercetin, kaempferol, myristin, apigenin, and luteolin also have antioxidative activity in many in vitro studies [45]. It has been observed that anthocyanins, which were one of the main antioxidant components in red wine, were the most effective, both in scavenging ROS and in inhibiting lipoprotein oxidation [46]. Quercetin is also known to have inhibited iron-catalyzed Fenton reaction (reaction between superoxide radicals with hydrogen peroxide).
\nThe exogenous (dietary) antioxidants are mainly derived from food and medicinal plants, such as fruits, vegetables, cereals, mushrooms, beverages, flowers, spices, and traditional medicinal herbs [47]. A large number of plant species and their phytochemicals have diverse medicinal properties, and almost majority of these plants have been found to possess excellent antioxidant activity within in vitro assays.
\nThe natural function of vitamin E which is present in vegetable oils, nuts, and other fatty plant-based foods is to prevent oxidation. Vitamin E therefore acts as antioxidant when consumed. It helps to prevent degradation of cell membranes in regions containing C〓C bonds. Some other antioxidants operate by different mechanisms, reacting with oxygen molecules (O2) to prevent the production of free radicals. Additionally, there are numerous dietary antioxidants that can be consumed which contribute to an enhanced cellular protection. Ascorbic acid, for example, effectively scavenges ROS and resynthesizes α-tocopherol [48].
\nSimilarly, a number of plants and plant isolates have been reported to protect free radical-induced damage in various experimental models. In recent times, focus on plant research has increased all over the world, and a large body of evidences has been collected to show the immense potential of medicinal plants used in various traditional systems. Green tea, for example, contains catechin components that are known to stimulate antioxidant activity by scavenging free radicals, inhibiting pro-oxidant enzymes and stimulating antioxidant enzymes [49]. Majority of these plants are endowed with free radical scavenging molecules, such as vitamins, terpenoids, phenolic acids, lignins, stilbenes, tannins, flavonoids, quinones, coumarins, alkaloids, amines, betalains, and other metabolites, which are rich in antioxidant activities [50].
\nVarious plant products have been used in the treatment of wounds over the years. Wound healing phytochemical compounds fight infection, promote blood clotting, and accelerate the healing process. Numerous phytochemical compounds have been identified and synthesized from medicinal plants that have unique properties associated with the mechanism of wound healing. Interestingly, many of these wound healing plants investigated displayed antioxidant potential as their major unique properties. A plethora of examples of medicinal plants appears in literature to have shown both wound healing and antioxidant properties.
\nIn my study of wound healing medicinal plants, 26 wound healing plants used among the people of Kpando Traditional Area for effective wound healing have been identified. In vitro investigations on four of these plants, namely,
The enhanced wound healing potency of various herbal extracts, therefore, may be partly attributed to free radical scavenging action of the phytoconstituents present in plant extracts.
\nMany plants used traditionally in treatment of wound possess antioxidant activity. It is evidently clear that wound healing and repair are accelerated by applying plant extracts that are rich in antioxidant phytochemicals. The assertion made that wound healing and antioxidant activity coexist, to some extent, can be confirmed. Researchers are encouraged to intensify their search for plants for the treatment of wounds with novel antioxidant activity that could be beneficial in therapeutic practice.
\nI am grateful to the University of Cape Coast for their support.
\nAuthor declared no conflict of interest.
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