Abstract
In order to achieve a hyperthyroid state, rats were treated for 7 days with thyroxine (150 microgram/100 g BW) or triiodothyronine (10 microgram/100 g BW). This regimen resulted in an enhanced activity of the microsomal ethanol oxidizing system. In addition, a decrease of hepatic alcohol dehydrogenase activity was observed under these experimental conditions, whereas hepatic catalase activity remained unchanged. These findings suggest that if chronic ethanol consumption simulates a functional "hyperthyroid hepatic state", increased rates of ethanol metabolism observed following prolonged alcohol intake might therefore be attributed at least in part to an induced activity of the microsomal ethanol oxidizing system in the liver.
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