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本文研究了大肠粘膜细胞和肝细胞微粒体酶系对专一性致大肠癌化合物—二甲基肼(DMH)的代谢活性。实验证明,大肠粘膜细胞如同肝细胞一样,存在依赖细胞色素P450的混合功能氧化酶,能催化DMH的羟化反应.使之转变成具直接致癌活性的终致癌物,其羟化活性大约相当于肝的79.5％。大肠粘膜细胞对DMH的羟化活性及细胞色素P450含量,能被苯巴比妥钠所诱导,如给动物以维生素E,则两者同时降低。文中强调了大肠粘膜细胞色素P450在DMH代谢转变中的重要作用,并讨论了维生素E在预防大肠化学致癌过程中的意义。
This study investigated the metabolic activity of colorectal mucosal cells and hepatocyte microsomal enzymes against the specific colorectal cancer compound, dimethylhydrazine (DMH). Experiments have shown that colonic mucosa cells, like liver cells, have mixed-function oxidases that depend on cytochrome P450, can catalyze the hydroxylation of DMH, turn it into a terminal carcinogen with direct carcinogenic activity, and its hydroxylation activity is approximately equivalent to 79.5% of the liver. The hydroxylation activity and cytochrome P450 content of DMH in colon mucosa cells can be induced by phenobarbital sodium. If vitamin E is given to animals, both of them decrease. This article emphasizes the important role of colorectal mucosa cytochrome P450 in the metabolism of DMH, and discusses the significance of vitamin E in the prevention of chemical carcinogenesis of large intestine.