Galtier P, Larrieu G, Lesca P
J Pharm Pharmacol. 1985 Oct;37(10):751-4. doi: 10.1111/j.2042-7158.1985.tb04960.x.
Adult, male rats were infected with 20 metacercariae of Fasciola hepatica given orally, other rats were left untreated. Five weeks after infestation, some animals received phenobarbitone, 3-methylcholanthrene, beta-naphthoflavone or Arochlor 1254, to induce liver drug metabolizing enzymes. Fascioliasis provoked decreases in aminopyrine N-demethylase, aniline hydroxylase, the mutagenic activity of cyclophosphamide and cytochrome P-450 concentration in untreated or phenobarbitone or Arochlor pretreated rats. In contrast, cytochrome b5, NADPH cytochrome c reductase, ethyoxycoumarin O-deethylase and the enzymatic activation of ethidium bromide were not affected by fascioliasis whatever pretreatment was given. Fascioliasis decreased liver drug metabolizing enzymes which were specifically induced by both phenobarbitone and Arochlor, this could be due to either the specific action of toxic excretions of flukes or to the particular localization of tissue damage within the liver lobule.
成年雄性大鼠经口感染20只肝片吸虫囊蚴,其他大鼠不做处理。感染后5周,部分动物给予苯巴比妥、3 - 甲基胆蒽、β - 萘黄酮或多氯联苯混合物1254,以诱导肝脏药物代谢酶。在未处理、经苯巴比妥或多氯联苯混合物预处理的大鼠中,肝片吸虫病导致氨基比林N - 脱甲基酶、苯胺羟化酶、环磷酰胺的诱变活性及细胞色素P - 450浓度降低。相比之下,无论给予何种预处理,细胞色素b5、NADPH细胞色素c还原酶、乙氧基香豆素O - 脱乙基酶及溴化乙锭的酶促活化均不受肝片吸虫病影响。肝片吸虫病降低了由苯巴比妥和多氯联苯混合物特异性诱导的肝脏药物代谢酶,这可能是由于吸虫有毒排泄物的特定作用,或是由于肝小叶内组织损伤的特定定位所致。