The carcinogenic mycotoxin aflatoxin B(1) (AFB(1)) induces 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation in mouse lung, an effect that can be prevented by treatment with polyethylene glycol-conjugated catalase (PEG-CAT). G-->T transversion mutation in K-ras, an early event in AFB(1)-induced mouse lung carcinogenesis, is thought to result from AFB(1)-8,9-exo-epoxide binding to DNA to form AFB(1)-N(7)-guanine, but may also result from formation of 8-OHdG. Therefore, oxidative DNA damage may be important in AFB(1) carcinogenicity.
View Article and Find Full Text PDFAflatoxin B(1) (AFB(1)) is a mycotoxin produced by some strains of Aspergillus and is a recognized pulmonary and hepatic carcinogen. The most widely accepted mechanism of AFB(1) carcinogenicity involves bioactivation to AFB(1)-8,9-exo-epoxide and binding to DNA to form AFB(1)-N(7)-guanine. Another potential cause of DNA damage is AFB(1)-mediated stimulation of reactive oxygen species formation, leading to oxidation of DNA bases.
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