吡唑对大鼠的处理增强了四氯化碳而非氯仿的肝毒性。

Pyrazole treatment of rats potentiates CCL4-but not CHCL3-hepatotoxicity.

作者信息

Ebel R E

机构信息

Department of Biochemistry and Nutrition, Virginia Polytechnic Institute, Blacksburg 24061.

出版信息

Biochem Biophys Res Commun. 1989 Jun 15;161(2):615-8. doi: 10.1016/0006-291x(89)92643-0.

DOI:10.1016/0006-291x(89)92643-0

PMID:2735913

Abstract

Rats were treated with pyrazole to increase the liver content of the "alcohol-inducible" form of cytochrome P-450. This treatment increased the sensitivity of these animals to CCl4-hepatotoxicity assessed by increases in SGPT and SGOT levels and decreases in microsomal cytochrome P-450 and aniline p-hydroxylase activity. However, the hepatotoxicity of CHCl3 was not increased by pyrazole-treatment. These data are consistent with the hypothesis that the "alcohol-inducible" form of cytochrome P-450 is capable of CCl4- but not CHCl3-activation.

摘要

用吡唑处理大鼠以增加细胞色素P - 450的“酒精诱导型”形式在肝脏中的含量。这种处理通过血清谷丙转氨酶（SGPT）和血清谷草转氨酶（SGOT）水平升高以及微粒体细胞色素P - 450和苯胺对羟基化酶活性降低来评估，增加了这些动物对四氯化碳肝毒性的敏感性。然而，吡唑处理并未增加三氯甲烷的肝毒性。这些数据与细胞色素P - 450的“酒精诱导型”形式能够激活四氯化碳而非三氯甲烷这一假设一致。