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• 基金项目：

• 杨端
• 中国科学院水生生物研究所

• 周仁珍
• 中国科学院水生生物研究所

• 摘要：用直接致癌物N-甲基亚硝基胍或需经酶活化才有活性的致癌原苯并（a）芘、苯并（a）蒽处理草鱼原代肝细胞培养物后,用放射自显影方法测出有明显的DNA修复合成。对照有标记³H-胸腺嘧啶核苷的细胞非常少,证明草鱼原代肝细胞中DNA复制水平很低。 ³H-胸腺嘧啶核苷掺入鱼原代肝细胞DNA的量与各种致癌物及致癌原的浓度有关。这表明鱼肝细胞有能力将致癌原代谢成能损伤DNA的致癌物,从而刺激DNA的修复。 BHC（六六六）可以诱导草鱼原代肝细胞培养物的DNA修复,但氯化镉没有活性。 本报告表明致癌物可诱导鱼肝细胞的DNA修复,因此它可以作为生物监测环境致癌物的补充手段。

• Abstract：When primary hepatocyte cultures of C. idellus were exposed to the direct-acting carcinogen, N-methyl-N-nitrosguanidin, and two procarci-nogens, benzo (a) pyrene and benzo (a)anthracene, it was possible to measure significant increase in DNA repair by autoradiography. The nuclear ³H-thymidine labelling index of control culture was small and the level of replication of the primary fish hepatocyte culture was very low.Treatment with different concentrations of various carcinogens and procarcinogens on cultured fish hepatocytes showed that the increase of ³H-thymidine incorporation into DNA was dose-dependent. These results demonstrate the ability of fish hepatocytes to metabolize prehe-patocarcinogens into forms that damaged DNA helps stimulate their repair.The induction of DNA repair in hepatocytes of primary cell culture of C. idellus was observed after exposure to BHC, but not after cadmium chloride.The present report shows that fish hepatocytes may prove to be an adequate supplemental biological monitor of carcinogens in the environment.

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