ABSENCE OF STIMULATION OF HEPATIC-MICROSOMAL ETHANOL OXIDIZING SYSTEM(MEOS) BY CHRONIC ETHANOL FEEDING IN RATS

Although in our previous studies on chronic alcoholism in rats some of the components of the hepatic microsomal ethanol oxidizing system (ME OS), such as P450 and NADPH cytochrome c reductase were not significan tly affected, the MEOS activity was not determined. The activity of th is system was studied in male Wistar rats (83-105 g) fed for 12-13 wee ks two almost similar basal diets, but one containing relatively high amounts of alpha-tocopherol, and the other relatively low levels of th is vitamin. The control groups were fed these basal diets and water ad lib, and the experimental rats the same basal diets plus a 32% ethano l - 25% sucrose mixture in the drinking fluid. The results showed that while in the ethanol fed rats consuming the diet relatively high in a lpha-tocopherol the MEOS activities were not significantly different f rom those of the corresponding control group, in the ethanol treated r ats fed the diet relatively low in this vitamin, the MEOS activities w ere significantly reduced in relation to the values in the correspondi ng control group. In our studies, as well as in those reported by othe r investigators, the hepatic activities of alcohol dehydrogenase (ADH) and catalase were not generally stimulated by the chronic consumption of ethanol. Since it has been shown that the chronic alcoholism in ma n and experimental animals is almost invariably associated with an inc rease in the ethanol metabolic rate (EMR), all these observations stro ngly suggested that this adaptive increase may not be due to any stimu lation of MEOS, ADH or catalase. The present results and a review of t he existing information on MEOS also suggested that the eventual stimu lation of this system may not be due to a direct effect of ethanol con sumption, but rather to dietary aberrations (i.e. high fat, low carboh ydrate regimens).