Gopalan P, Tsuji K, Lehmann K, Kimura M, Shinozuka H, Sato K, Lotlikar P D
Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA 19140.
Carcinogenesis. 1993 Jul;14(7):1469-70. doi: 10.1093/carcin/14.7.1469.
Induction of glutathione S-transferase placental form (GST-P) positive hepatic foci has been examined by immunohistochemical analysis in young male Fischer rats 3 weeks after a single i.p. injection of aflatoxin B1 (AFB1). Pretreatment of rats with L-buthionine sulfoximine (BSO), a GSH depleter, at a dose of 4 mmol/kg body wt 4 and 2 h before 1.0 mg AFB1 treatment enhanced both the number of AFB1-induced hepatic foci and the area occupied by these foci by approximately 400 and 575% above their respective controls without affecting the mean diameter of these foci. Pretreatment of rats with 0.1% phenobarbital (PB) in their drinking water for 1 week before AFB1 (1 mg) treatment, inhibited AFB1-induced foci almost completely. However, the number of AFB1-induced foci in PB-pretreated rats was not significantly increased by BSO pretreatment.
通过免疫组织化学分析,在年轻雄性Fischer大鼠经腹腔单次注射黄曲霉毒素B1(AFB1)3周后,检测谷胱甘肽S-转移酶胎盘型(GST-P)阳性肝灶的诱导情况。在1.0 mg AFB1处理前4小时和2小时,以4 mmol/kg体重的剂量用谷胱甘肽耗竭剂L-丁硫氨酸亚砜胺(BSO)对大鼠进行预处理,AFB1诱导的肝灶数量及其所占面积比各自的对照组分别增加了约400%和575%,而这些肝灶的平均直径未受影响。在AFB1(1 mg)处理前1周,用0.1%苯巴比妥(PB)的饮水对大鼠进行预处理,几乎完全抑制了AFB1诱导的肝灶。然而,BSO预处理并未使PB预处理大鼠中AFB1诱导的肝灶数量显著增加。