Saito M, Nagayama S, Ikegami S, Innami S
Division of Food Science, National Institute of Health and Nutrition, Tokyo, Japan.
Int J Vitam Nutr Res. 1990;60(3):255-60.
The present study is carried out to explore whether the liver microsomal drug-metabolizing enzymes induced by PCB are associated with the PCB-induced liver lipid peroxide formation in rats. For this purpose, variations of the drug-metabolizing enzyme activities mediated by vitamin B2 deficiency were utilized. The administration of PCB to rats induced the liver microsomal cytochrome P-450 and vitamin B2 deficiency promoted the induction. The cytochrome b5 was also induced by PCB but no further induction by vitamin B2 deficiency was observed. The flavoenzyme, NADPH-cytochrome c reductase, was induced by PCB when the vitamin B2-supplemented PCB diet was fed to rats, but the activity of the enzyme was decreased by vitamin B2 deficiency and PCB further decreased the activity. The liver lipid peroxide levels increased in PCB groups with and without vitamin B2 compared with each PCB-free group, but the lipid peroxide level in vitamin B2-deficient PCB group was significantly lower than in vitamin B2-supplemented PCB group. From these results, the PCB-induced liver lipid peroxide formation was not necessarily related to the variations of the liver microsomal drug-metabolizing enzymes.
本研究旨在探讨多氯联苯诱导的大鼠肝脏微粒体药物代谢酶是否与多氯联苯诱导的肝脏脂质过氧化物形成有关。为此,利用了由维生素B2缺乏介导的药物代谢酶活性变化。给大鼠施用多氯联苯可诱导肝脏微粒体细胞色素P-450,维生素B2缺乏会促进这种诱导作用。细胞色素b5也可被多氯联苯诱导,但未观察到维生素B2缺乏会进一步诱导其产生。当给大鼠喂食补充了维生素B2的多氯联苯饮食时,黄素酶NADPH-细胞色素c还原酶可被多氯联苯诱导,但该酶的活性会因维生素B2缺乏而降低,多氯联苯会进一步降低其活性。与每个无多氯联苯组相比,补充和未补充维生素B2的多氯联苯组的肝脏脂质过氧化物水平均升高,但维生素B2缺乏的多氯联苯组的脂质过氧化物水平明显低于补充维生素B2的多氯联苯组。从这些结果来看,多氯联苯诱导的肝脏脂质过氧化物形成不一定与肝脏微粒体药物代谢酶的变化有关。