蒽醌 -2-磺酸对大鼠肝微粒体的主要毒性作用。

Primary toxic effects of anthraquinone-2-sulfonic acid in rat liver microsomes.

作者信息

Leskovac V, Trivić S, Peggins J O

机构信息

Faculty of Technology, Novi Sad, Yugoslavia.

出版信息

Toxicol Lett. 1995 Jul;78(2):107-10. doi: 10.1016/0378-4274(94)03238-3.

DOI:10.1016/0378-4274(94)03238-3

PMID:7618176

Abstract

(1) The endogenous, NADPH-supported production of H2O2 and of O2-.-radicals in rat liver microsomes was very strongly enhanced in the presence of anthraquinone-2-sulfonic acid (AQSA). (2) This induction of H2O2 and of O2-.-radicals was catalyzed by the microsomal NADPH:cytochrome P450 oxidoreductase (EC 1.6.2.4). (3) AQSA was reduced to AQSA radicals by reductase; AQSA radicals reduce molecular oxygen to O2-.-radicals, which are readily dismutated to H2O2 by the microsomal superoxide dismutase. (4) O2-.-radicals are the sole precursors of all AQSA-induced production of H2O2 in liver microsomes.

摘要

(1) 在蒽醌 - 2 - 磺酸（AQSA）存在的情况下，大鼠肝微粒体中由内源性NADPH支持的H2O2和超氧阴离子自由基（O2 -·）的产生显著增强。(2) 微粒体NADPH：细胞色素P450氧化还原酶（EC 1.6.2.4）催化了这种H2O2和超氧阴离子自由基（O2 -·）的诱导产生。(3) 还原酶将AQSA还原为AQSA自由基；AQSA自由基将分子氧还原为超氧阴离子自由基（O2 -·），后者很容易被微粒体超氧化物歧化酶歧化为H2O2。(4) 超氧阴离子自由基（O2 -·）是肝微粒体中所有AQSA诱导产生H2O2的唯一前体。