Hepatic microsomal ethanol-oxidizing system (MEOS): increased activity following propylthiouracil administration.
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.