Sun Y, Li Y
Department of Biochemistry, Zhejiang Medical University, Hangchou, The People's Republic of China.
Cancer Lett. 1988 Feb;39(1):69-76. doi: 10.1016/0304-3835(88)90041-9.
The kinetic change of beta-glucuronidase (beta-G) activity was measured in mouse large intestinal mucosa during dimethylhydrazine (DMH) carcinogenesis with addition of cholic acid and/or indole. The experiment lasted 21 weeks. The enzyme activity began to increase significantly at 5th week after treatment of DMH with cholic acid and/or indole, and at 7th week with DMH alone. Then, increased activity remained the rest of the time. Mouse intestinal cancer induced by DMH injection are also shown to have an increased beta-G activity. The induction of beta-G activity in the early stage of DMH colon carcinogenesis and additive effects of cholic acid and/or indole may imply one mechanism of action of DMH as a carcinogen and cholic acid as a promoter in large intestinal cancer.
在添加胆酸和/或吲哚的情况下，测定了二甲基肼（DMH）致癌过程中小鼠大肠黏膜中β-葡萄糖醛酸酶（β-G）活性的动力学变化。实验持续了21周。在用胆酸和/或吲哚处理DMH后第5周，以及单独用DMH处理后第7周，酶活性开始显著增加。然后，在其余时间活性持续增加。DMH注射诱导的小鼠肠道癌也显示出β-G活性增加。DMH结肠致癌早期β-G活性的诱导以及胆酸和/或吲哚的相加作用可能意味着DMH作为致癌物和胆酸作为大肠癌促进剂的一种作用机制。
