Metcalfe S A, Neal G E
Carcinogenesis. 1983 Aug;4(8):1007-12. doi: 10.1093/carcin/4.8.1007.
Isolated rat hepatocytes, an intact cellular system capable of performing phase I and phase II metabolism, have been used to investigate metabolism of aflatoxin B1. These cells were found to metabolise [14C]aflatoxin B1 to aflatoxins M1 and Q1, and to radiolabelled polar material, presumably conjugates, as analysed by h.p.l.c., t.l.c. and radioactive determination. In vivo administration of the mixed function oxidase inducers, phenobarbitone and 3-methylcholanthrene, resulted in enhanced hepatocyte phase I (microsomal) metabolism of aflatoxin B1. In contrast to metabolism of AFB1 by in vitro subcellular systems increased production of polar material (conjugated metabolites) derived from [14C]aflatoxin B1 was also detected in hepatocytes isolated from these pretreated animals. Formation of aflatoxin Q1 by isolated hepatocytes appeared to be mediated by cytochrome P450-linked enzymes whereas cytochrome P448-linked enzymes were apparently involved in aflatoxin M1 production. Chronic feeding of aflatoxin B1 to rats enhanced hepatocyte production of conjugated material only and did not elevate cellular cytochrome P450 levels, thus suggesting that aflatoxin B1 is not an inducer of its own primary metabolism.
离体大鼠肝细胞是一种能够进行I相和II相代谢的完整细胞系统,已被用于研究黄曲霉毒素B1的代谢。通过高效液相色谱法(h.p.l.c.)、薄层层析法(t.l.c.)和放射性测定分析发现,这些细胞可将[14C]黄曲霉毒素B1代谢为黄曲霉毒素M1和Q1以及放射性标记的极性物质(可能是结合物)。体内给予混合功能氧化酶诱导剂苯巴比妥和3-甲基胆蒽,可增强肝细胞对黄曲霉毒素B1的I相(微粒体)代谢。与体外亚细胞系统对黄曲霉毒素B1的代谢情况不同,从这些预处理动物分离出的肝细胞中也检测到源自[14C]黄曲霉毒素B1的极性物质(结合代谢物)产量增加。离体肝细胞形成黄曲霉毒素Q1似乎是由细胞色素P450相关酶介导的,而细胞色素P448相关酶显然参与了黄曲霉毒素M1的生成。给大鼠长期喂食黄曲霉毒素B1仅增强了肝细胞结合物的生成,并未提高细胞色素P450水平,因此表明黄曲霉毒素B1不是其自身主要代谢的诱导剂。