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As we age, the Teriflunomide oxidative andor nitrosative damages elicit a number of lateonset diseases after ROSRNS accumulate to certain levels.Amongst the different organs in the body, the brain is particularly vulnerable to oxidative stress due to its high oxygen utilization, weaker antioxidant enzymes, high content of easily oxidized polyunsaturated fatty acids, and the terminaldifferentiation characteristic of neurons.This review focuses on the role of oxidative stress on neurodegenerative diseases.To aid the understanding of toxic targets in neurodegenerative diseases, this review begins with the essential characteristics of ROS, including its generation, regulation and physiological functions.Then, the mechanisms for ROS underlying neurodegeneration are highlighted with a focus on the causal relationship between ROS and protein misfolding and aggregation. In addition, the role of ROS in artificial eventinduced neuronal disorders, such as chemotherapyinduced cognitive impairment is assessed.The review further comments on drug developmental strategies for the therapy of neurodegenerative diseases, as well as prevention of anticancer druginduced neuronal disorders.The review closes with an evaluation of methodology that has been applied to measure oxidativenitrosative stress.These include different forms of nitric oxide. Reactive oxygen species can be generated from various sites in a cell.The cell protects its own damage from excessive ROS by suppression of ROS levels by two redox buffers and antioxidant enzymes, including superoxide dismutase. In the cell, superoxide dismutase enzymatically converts HO is into HO and O.In the TRX buffering system, the TRX in reduced status during the degradation of HO and then reduced by TR.Cells constantly generate ROS in mitochondria during aerobic metabolism.Under normal condition, of electrons leak from the mitochondrial electron transport chain and form O by cycling the ubiquinol in the inner mitochondrial membrane.In the cytosol, xanthine oxidase provides Secnidazole another enzymatic source to and HO. In addition, O is produced nonenzymatically by transferring a single produce both O electron to oxygen by reduced coenzymes, prosthetic groups or previously reduced xenobiotics. O is the precursor of most ROS and a mediator in oxidative chain reactions.In contrast to these, mitochondrial NOS, the isoform of nNOS, is located in the mitochondria where coexistence of NO and O results in the formation of ONOO.Thioredoxin reductase is also essential for keeping low levels of HO by converting it into HO and O as well. CAT, another enzyme that could convert HO to HO and O, is present in the cells of all aerobic bacteria, plants and animals.In addition to the enzymatic defense systems, the human body also uses nonenzymatic antioxidants to limit overaccumulation of ROS.These include, but are not limited to, ascorbic acid and flavonoids. Vitamin C is a potent antioxidant that neutralizes free radicals by donating an electron.Vitamin E is a fatsoluble vitamin whose main antioxidant function is protection against lipid peroxidation, providing a high efficiency antioxidant effect by stopping ROS from forming in membranes undergoing lipid peroxidation.GSH is highly abundant in the cytoplasm, nuclei and mitochondria.GSH reacts with a radical and becomes a thiyl radical itself.The newlygenerated thiyl radicals dimerize to form the nonradical product oxidized glutathione. Flavonoids stop the oxidation of lipids and other molecules by the rapid donation of hydrogen atoms to radicals, becoming the phenoxy radical intermediates by themselves.

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