Foliot A, Touchard D, Myara A, Trivin F, Chauffert M
Biochem Pharmacol. 1987 Aug 15;36(16):2617-20. doi: 10.1016/0006-2952(87)90540-5.
Administration of phenobarbital, a known inducer of glutathione S-transferase activity in rat liver, failed to stimulate sulfobromophthalein (BSP) conjugation by liver cytosol in hamsters. The latter displayed poor ability to conjugate this substrate, despite very high glutathione-conjugating activity with the broad-spectrum substrate 1-chloro-2,4-dinitrobenzene (CDNB). Of the six substrates tested, in this species, 1,2-epoxy-3-(4-nitrophenoxy)propane (ENPP) was the only one whose conjugation was greatly enhanced by phenobarbital (+172%). Nevertheless, hamsters proved as responsive to phenobarbital induction as rats, since it increased their relative liver weight and microsomal enzyme activity. The deficient induction of liver BSP-conjugating activity observed with phenobarbital is consistent with the finding that it did not affect the hepatic transport of this substrate in hamsters.
已知苯巴比妥可诱导大鼠肝脏谷胱甘肽S-转移酶活性，但它未能刺激仓鼠肝脏细胞溶质对磺溴酞钠（BSP）的结合作用。尽管仓鼠对广谱底物1-氯-2,4-二硝基苯（CDNB）具有非常高的谷胱甘肽结合活性，但它们对该底物的结合能力较差。在该物种测试的六种底物中，1,2-环氧-3-(4-硝基苯氧基)丙烷（ENPP）是唯一一种其结合作用因苯巴比妥而大幅增强的底物（增加了172%）。然而，仓鼠对苯巴比妥诱导的反应与大鼠一样，因为苯巴比妥增加了它们的相对肝脏重量和微粒体酶活性。苯巴比妥对仓鼠肝脏BSP结合活性的诱导不足，这与它不影响该底物在仓鼠肝脏中的转运这一发现是一致的。
