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Oxidative DNA Damage Induced by Ethanol in Mouse Peripheral Leucocytes
Author(s) -
Guo Lei,
Yang Jing Yu,
Wu Chun Fu
Publication year - 2008
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2008.00258.x
Subject(s) - comet assay , oxidative stress , ethanol , dna damage , reactive oxygen species , genotoxicity , antioxidant , deoxyguanosine , chemistry , 8 hydroxy 2' deoxyguanosine , oxidative phosphorylation , pharmacology , biochemistry , dna , toxicity , dna oxidation , biology , organic chemistry
It is suggested that reactive oxygen species produced during ethanol intake may induce oxidative DNA damage. The present study, by the use of single cell gel electrophoresis (comet assay), investigated the potential genotoxicity of acute and long‐term ethanol administration in mouse peripheral leucocytes. Urinary 8‐hydroxy‐2′‐deoxyguanosine and total antioxidant capacity and reactive oxygen species in whole blood were also detected. Acute or long‐term administration of ethanol, at the dose of 2.5 or 5.0 g/kg intraperitoneally, for 30 days, could induce significant DNA damage in peripheral leucocytes, which could be repaired at least 3 days after ethanol withdrawal in long‐term ethanol treatment. A significant increase of urinary 8‐hydroxy‐2′‐deoxyguanosine and generations of reactive oxygen species in whole blood after ethanol administration were observed, which demonstrated the ethanol‐induced oxidative DNA damage. Interestingly, it was found that the total antioxidant capacity was significantly increased in whole blood after long‐term ethanol administration compared to the control group, which suggested enhancement in the activities of the antioxidative defence system against oxidative tissue damage caused by excessive ethanol consumption. Thus, the present studies provide a clear evidence that ethanol induced DNA damage in peripheral leucocytes, which might result from ethanol‐induced oxidative stress in the body.