Chapters authored
Dietary Antioxidants in Experimental Models of Liver Diseases
Oxidative stress is caused by the imbalance between the amount of reactive oxygen species (ROS) and antioxidant capacity in the body. A balanced diet involving the daily intake of antioxidant-rich foods makes improvements in the total antioxidant capacity of individuals and would therefore reduce the incidence of oxidation-related diseases. It may also regulate the degree of oxidative stress. In fact, dietary micronutrients are either direct antioxidants or components of antioxidant enzymes, which may contribute positively to certain indicators of hepatic function. Liver plays an important role in the regulation of various processes such as metabolism, secretion, storage, and the clearance of endogenous and exogenous substances. Once liver is damaged by pursuing a wrong diet and inflammation takes place, most of these physiological functions get altered. Apart from drugs that used to treat the ailments, it is also necessary to determine the pharmaceutical alternatives for the drugs that are used in the treatment of liver diseases. Therefore, this chapter aims to summarize all known information on the effects of dietary nutrients on oxidative stress in experimental liver models.
Part of the book: Strawberry
Lipid Peroxidation
Lipid peroxidation (LPO) is initiated by the attack of free radicals (eg OH ·, O2- and H2O2) on cellular or organelle membranes phospholipids or polyunsaturated fatty acids (PUFA), and with the formation of various types of aldehydes, ketones, alkanes, carboxylic acids and polymerization products. It is an autoxidation process that results. These products are highly reactive with other cellular components and serve as biological markers of LPO. Malondialdehyde (MDA), a toxic aldehyde end product of LPO, causes structural changes that mediate its oxidation, such as fragmentation, modification, and aggregation, especially in DNA and protein. The excessive binding of these reactive aldehydes to cellular proteins alters membrane permeability and electrolyte balance. Degradation of proteins leads to progressive degradation of the biological system mediated by oxidative stress. The chain reaction (CR) of LPO is initiated by the attack of free radicals on the PUFA of the cell membrane to form a carbon centered radical (R*). The O2 · - radical attacks the other lipid molecule to form lipid hydroperoxide (ROOH), thereby spreading the CR and forming the lipid peroxyl radical (ROO). These lipid hydroperoxides severely inhibit membrane functionality by allowing ions such as increased hardness and calcium to leak through the membrane. Damage to the lipid membrane and macromolecule oxidation can result in activation of necrotic or apoptotic tissue death pathways if severe enough.
Part of the book: Accenting Lipid Peroxidation