Nousiainen U, Törrönen R, Hänninen O
Toxicology. 1984 Sep 14;32(3):243-51. doi: 10.1016/0300-483x(84)90077-5.
Hepatic and extrahepatic carboxylesterase (EC 3.1.1.1) activities were studied after the exposure of rats to polycyclic aromatic hydrocarbons. In dose- and time-dependent studies, the carcinogens benz[a]anthracene, benzo[a]pyrene and 3-methylcholanthrene moderately induced the hepatic cytosolic and kidney microsomal carboxylesterase activities, while the non-carcinogenic compounds anthracene, phenanthrene and chrysene had no effects on these enzyme activities. The hepatic microsomal and kidney cytosolic enzyme activities were not altered by the polycyclic aromatic hydrocarbons tested. Carboxylesterase activity in the postmitochondrial fraction of the intestinal mucosa decreased the serum enzyme activity slightly increased after the administration of the carcinogenic compounds. Although the in vitro hydrolysis of propanidid by hepatic cytosolic and kidney microsomal preparations was increased, the biological half-life of propanidid in vivo was not changed by 3-methylcholanthrene treatment.
在大鼠接触多环芳烃后，对其肝脏和肝外羧酸酯酶（EC 3.1.1.1）活性进行了研究。在剂量和时间依赖性研究中，致癌物苯并[a]蒽、苯并[a]芘和3-甲基胆蒽适度诱导了肝脏胞质和肾脏微粒体羧酸酯酶活性，而非致癌化合物蒽、菲和 Chrysene对这些酶活性没有影响。所测试的多环芳烃未改变肝脏微粒体和肾脏胞质酶活性。肠道黏膜线粒体后组分中的羧酸酯酶活性在给予致癌化合物后略有下降，血清酶活性略有增加。尽管肝脏胞质和肾脏微粒体制剂对丙泮尼地的体外水解增加，但3-甲基胆蒽处理并未改变丙泮尼地在体内的生物半衰期。
