DNA damage checkpoint response to aflatoxin B1.

摘要: Although most countries regulate the aflatoxin levels in food by legislations, high amounts of B1 (AFB1)-DNA adducts can still be detected normal and tumorous tissue obtained from cancer patients. AFB1 cannot directly interact with DNA unless it is biotransformed to AFB1-8, 9-epoxide via cytochrome p450 enzymes. This metabolite spontaneously irreversibly attaches guanine residues generate highly mutagenic adducts. AFB1-induced mutation ATM kinase results deterioration cell cycle checkpoint activation at G2/M site. Genomic instability increased risk due A-T result diminished repair double strand breaks. The major point caused G-to-T transversion that related frequency p53 mutation. Majority associated hepatocellular cases carry TP53 mutant DNA, which an indicator exposure, as well risk.