Moreno F, Petrides A S, Heinen E, Strohmeyer G, Teschke R
Alcohol Clin Exp Res. 1981 Jan;5(1):85-91. doi: 10.1111/j.1530-0277.1981.tb04870.x.
Treatment for 7 days with the thyreostatic drug propylthiouracil (5 mg/100 g of body weight) resulted in a hypothyroid hepatic state as shown by the marked decreased hepatic content of thyroxine and triiodothyronine. This regimen led to an enchanced activity of the microsomal ethanol-oxidizing system, whereas the activities of alcohol dehydrogenase and catalase remained unchanged. Moreover, a hyperthyroid hepatic state achieved following the daily administration of L-thyroxine (150 micrograms/100 g of body weight) or L-3,3', 5-triiodothyronine (10 micrograms/100 g body weight) for 7 days resulted in a similar increased activity of the microsomal ethanol-oxidizing system. Under these conditions, a decrease of alcohol dehydrogenase activity and an unaffected catalase activity was observed. These findings, therefore, show that the administration of either propylthiouracil or thyroid hormones results in an increased activity of the microsomal ethanol-oxidizing system, suggesting that the underlying mechanism for the induction of the microsomal ethanol-oxidizing system by propylthiouracil is independent of the action of thyroid hormones.
用甲状腺抑制剂丙硫氧嘧啶（5毫克/100克体重）治疗7天导致甲状腺功能减退的肝脏状态，表现为肝脏中甲状腺素和三碘甲状腺原氨酸含量显著降低。这种治疗方案导致微粒体乙醇氧化系统的活性增强，而乙醇脱氢酶和过氧化氢酶的活性保持不变。此外，每天给予L-甲状腺素（150微克/100克体重）或L-3,3',5-三碘甲状腺原氨酸（10微克/100克体重）7天所达到的甲状腺功能亢进的肝脏状态，也导致微粒体乙醇氧化系统的活性出现类似增加。在这些条件下，观察到乙醇脱氢酶活性降低，而过氧化氢酶活性未受影响。因此，这些发现表明，给予丙硫氧嘧啶或甲状腺激素都会导致微粒体乙醇氧化系统的活性增加，这表明丙硫氧嘧啶诱导微粒体乙醇氧化系统的潜在机制与甲状腺激素的作用无关。
