期刊
TRENDS IN CARDIOVASCULAR MEDICINE
卷 11, 期 3-4, 页码 148-155出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/S1050-1738(01)00094-9
关键词
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资金
- NCI NIH HHS [CA65878] Funding Source: Medline
Reactive oxygen species can directly cause covalent modifications to DNA. Alternatively, they can initiate the formation of lipid hydroperoxides, which undergo homolytic decomposition to the alpha,beta -unsaturated aldehyde genotoxins, 4-oxo-2-nonenal, 4,5-epoxy-2(E)-decenal, and 4-hydroxy-2-nonenal through two quite separate pathways. One pathway involves a complex rearrangement of the alkoxy radical derived from the lipid hydroperoxide. The other pathway involves the intermediate formation of 4-hydroperoxy-2-nonenal. Lipid hydroperoxides can also be derived from the action of lipoxygenases and cyclo-oxygenases on polyunsaturated fatty acids. 4,5-Epoxy-2(E)-decenal forms etheno-2 ' -deoxyadenosine adduct with DNA, a mutagenic lesion observed in human tissue DNA samples. Several new ethano- and etheno-DNA adducts have been identified from the reaction of 4-oxo-2-nonenal with DNA. Malondialdehyde, another genotoxic bifunctional electrophile, forms a propano adduct with 2 ' -deoxyguanosine (M(1)G-dR) rather than an etheno adduct. Very little is known about the consequences of lipid hydroperoxide-mediated DNA damage in cardiovascular diseases. This should prove to be an important area for future research. (C) 2001, Elsevier Science Inc.
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