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Hepatic Microsomal Ethanol‐Oxidizing System (MEOS): Increased Activity Following Propylthiouracil Administration
Author(s) -
Moreno Fernando,
Petrides Alexander S.,
Heinen Edgar,
Strohmeyer Georg,
Teschke Rolf
Publication year - 1981
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1981.tb04870.x
Subject(s) - propylthiouracil , medicine , endocrinology , microsome , triiodothyronine , chemistry , ethanol , catalase , alcohol dehydrogenase , oxidizing agent , hormone , thyroid , enzyme , biochemistry , organic chemistry
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 enhanced 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 jig/100 g of body weight) or L‐3,3′, 5‐triiodothyronine (10 pg/100 g of 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.