Shen H M, Ong C N, Lee B L, Shi C Y
Department of Community, Occupational and Family Medicine, National University of Singapore.
Carcinogenesis. 1995 Feb;16(2):419-22. doi: 10.1093/carcin/16.2.419.
A time- and dose-dependent increase in 8-hydroxydeoxyguanosine (8-OHdG) was observed in rat hepatic DNA after a single i.p. injection of aflatoxin B1 (AFB1). It was also found that pre-treatment with selenium or deferoxamine significantly reduced 8-OHdG level in AFB1-administered rats. In contrast, no reduction in 8-OHdG concentration was found in vitamin E-pre-treated rats. These results provide evidence that AFB1 causes oxidative DNA damage in rat liver, which may involve hydroxyl radicals as the initiating species. It is postulated that AFB1-induced oxidative DNA damage (8-OHdG formation) may constitute an important pathway in AFB1 hepatocarcinogenesis.
单次腹腔注射黄曲霉毒素B1(AFB1)后,在大鼠肝脏DNA中观察到8-羟基脱氧鸟苷(8-OHdG)呈时间和剂量依赖性增加。还发现,用硒或去铁胺预处理可显著降低给予AFB1的大鼠体内的8-OHdG水平。相比之下,维生素E预处理的大鼠体内8-OHdG浓度没有降低。这些结果证明AFB1会在大鼠肝脏中引起氧化性DNA损伤,这可能涉及羟基自由基作为起始物种。据推测,AFB1诱导的氧化性DNA损伤(8-OHdG形成)可能是AFB1诱导肝癌发生的一条重要途径。