Chronic alcohol consumption prevents 8-hydroxyguanine accumulation in 3′-methyl-4-dimethylaminoazobenzene-treated mouse liver

Alcohol consumption is known to have opposing effects on carcinogenesis: promotion and prevention. In this study, we examined the effects of 12% ethanol on oxidative DNA damage accumulation and its repair in mouse livers treated with 3′-methyl-4-dimethylaminoazobenzene (3′-MeDAB), a well-known hepatic carcinogen. We previously reported that 3′-MeDAB increased 8-hydroxyguanine (8-OH-Gua) accumulation and its repair activity, accompanied by the fragmentation of 8-oxoguanine DNA glycosylase 1 (OGG1), the main repair enzyme of 8-OH-Gua. The present results showed that 12% ethanol intake attenuated the 8-OH-Gua accumulation, but not the fragmentation of OGG1 induced by 3′-MeDAB. Additionally, no significant changes in oxidative status, as monitored by lipid peroxidation (LPO), were observed among the 3′-MeDAB-treated mouse livers with/without alcohol administration. These findings suggested that 12% ethanol consumption may reduce the risk of 3′-MeDAB-induced carcinogenesis by decreasing 8-OH-Gua accumulation.