虹鳟鱼肝微粒体混合功能单加氧酶对2,5-二苯基恶唑（PPO）的代谢作用

Metabolism of 2,5-diphenyloxazole (PPO) by trout liver microsomal mixed function monooxygenase.

作者信息

Ahokas J T

出版信息

Res Commun Chem Pathol Pharmacol. 1976 Mar;13(3):439-47.

Abstract

Metabolism of 2,5-diphenyloxazole (PPO) has been characterized in trout liver microsomes. Trout liver microsomes have been found to metabolize PPO into at least one NaOH extractable flourescing metabolite having a strong excitation peak at 345 nm and an emission peak at about 510 nm. As the metabolite(s) has (have) not been characterized, Vmax has not been determined, however in arbitary fluorescent units (FU) Vmax is several fold higher in the trout than in the male rat hepatic microsomes. Km is 12.7 M, being about twice as high as reported for mouse (Cantrell et al. 1975). Optimum assay conditions have been established for the metabolism of PPO by trout liver microsomes. NADPH generating system is essential and the metabolism was strongly inhibited by alpha-naphthoflavone, but much less markedly by SKF 525 A or metyrapone.

摘要

已对虹鳟鱼肝微粒体中2,5 - 二苯基恶唑（PPO）的代谢进行了表征。已发现虹鳟鱼肝微粒体将PPO代谢为至少一种可被氢氧化钠提取的荧光代谢物，该代谢物在345 nm处有一个强激发峰，在约510 nm处有一个发射峰。由于该代谢物尚未得到表征，所以尚未确定Vmax，然而，以任意荧光单位（FU）计，虹鳟中的Vmax比雄性大鼠肝微粒体中的高几倍。Km为12.7 μM，约为报道的小鼠的两倍（坎特雷尔等人，1975年）。已确定了虹鳟鱼肝微粒体代谢PPO的最佳测定条件。NADPH生成系统必不可少，该代谢受到α - 萘黄酮的强烈抑制，但受到SKF 525 A或甲吡酮的抑制则明显较弱。