Santhanam K, Lotlikar P D
Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA 19140.
Cancer Lett. 1989 May;45(2):129-34. doi: 10.1016/0304-3835(89)90147-x.
The effect of beta-naphthoflavone (BNF) pretreatment of hamsters on the hepatic metabolism of aflatoxin B1 (AFB1) has been examined in studies in vitro and in vivo. Pretreatment with BNF not only increased microsomal cytochrome P-450 by 50-80% but also increased microsome-mediated AFB1 epoxidation as measured by AFB1-DNA binding 2.6 fold without significantly affecting other hydroxylations. Neither cytosolic GSH S-transferases' activities nor AFB1-GSH (AFB1-SG) conjugation were affected. In vivo, hepatic AFB1-DNA binding was also increased about 3-4-fold. These results in contrast to those observed in the rat indicate that induced species of cytochrome P-450 are primarily responsible for higher epoxidation of AFB1 in the hamster.
在体外和体内研究中，已检测了用β-萘黄酮（BNF）预处理仓鼠对黄曲霉毒素B1（AFB1）肝脏代谢的影响。用BNF预处理不仅使微粒体细胞色素P-450增加了50 - 80%，而且通过AFB1-DNA结合测定，微粒体介导的AFB1环氧化增加了2.6倍，而对其他羟基化反应没有显著影响。胞质谷胱甘肽S-转移酶的活性和AFB1-谷胱甘肽（AFB1-SG）结合均未受影响。在体内，肝脏AFB1-DNA结合也增加了约3 - 4倍。这些结果与在大鼠中观察到的结果相反，表明诱导产生的细胞色素P-450同工酶是仓鼠中AFB1更高环氧化反应的主要原因。
