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- W2479937589 startingPage "319" @default.
- W2479937589 abstract "Cells in an aerobic environment generate reactive oxygen and reactive nitrogen species, which have the potential to cause significant damage to cell organelles and individual proteins. Oxidant stress can compromise cell function and ultimately cause cell death. Relevant intracellular sources of reactive oxygen formation include the electron transport chain of mitochondria, the P-450 system in microsomes, and various oxidases in peroxisomes and in the cytosol. An important source of superoxide and other oxidants released into endosomes or to the outside is the family of NADPH oxidases (NOXs). In order to survive in this environment, cells have developed a sophisticated system of enzymes and small molecules that limit the formation of highly reactive oxygen species and effectively detoxify them. This system includes superoxide dismutases, glutathione peroxidases, catalase, thioredoxins, and peroxiredoxins in various cell organelles. In addition, water–soluble antioxidants such as glutathione and lipid–soluble antioxidants such as tocopherols and carotenoids are critical cofactors or direct scavengers of various oxidants. Another strategy to limit oxidant-induced tissue damage is to keep the levels of unbound transition metals in the cell extremely low through effective chelation by storage and transport proteins such as ferritin, transferrin, and ceruloplasmin. This chapter summarizes our current knowledge of reactive oxygen formation, the defense systems that control these oxidants, and their pathophysiological relevance in the liver." @default.
- W2479937589 created "2016-08-23" @default.
- W2479937589 creator A5087156903 @default.
- W2479937589 date "2010-01-01" @default.
- W2479937589 modified "2023-09-23" @default.
- W2479937589 title "Antioxidant Defense Mechanisms" @default.
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