Oxidative stress is an inevitable consequence of aerobic life. Oxidative damage to deoxyribonucleic acid (DNA) and other biomolecules accumulates with age and has been implicated in age-related degenerative diseases and cancer (1) . Reactive oxygen species, including superoxide anion, hydrogen peroxide (H 2 O 2 ), hydroxyl radical, and singlet oxygen, are generated as by-products of aerobic metabolism, as well as by exposure to various natural and synthetic toxicants and ultraviolet/ionizing radiation. Reactive oxygen species can attack DNA to form cytotoxic and mutagenic lesions. The most frequently measured oxidized DNA product, 8-oxo-deoxyguanosine (or 8-OH-dG), may be formed by the direct attack of highly reactive hydroxyl radicals on the guanine residues in DNA. Oxygen radicals may also initiate autocatalytic lipid peroxidation, giving rise to additional reactive species, such as lipid epoxides, lipid hydroperoxides, lipid alkoxyl and peroxyl radicals, and aldehydes. Besides oxidative damage, reactive oxygen species can act as secondary messengers to induce the expression of a variety of transcriptional factors involved in stress responses and pathological processes. Fortunately, mammalian cells have several levels of antioxidant defense against constant infusion of reactive oxygen species by maintaining a pro-oxidant/antioxidant balance. The glutathione redox system appears to be essential in antioxidant
The American Journal of Medicine – Elsevier
Published: Jun 1, 2003
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