Chronic alcohol intoxication led to an increase in activity of alcohol dehydrogenase and to decrease -- of aldehyde dehydrogenase and the microsomal ethanol oxidizing system (MEOS) with simultaneous activation of cytochrome P-450 in liver tissue of rats during ontogenesis. Ethanol, which did not affect the enzymatic status of lysosomes within ontogenesis (alpha- and beta-glucosidases, alpha- and beta-galactosidases, alpha-mannosidase, beta-N-acetylglucosaminidase, beta-xylosidase, beta-glucuronidase, beta-N-acetyl galactosaminidase acid RNAase, arylsulfatases A and B, cathepsin D), activated the majority of hydrolases in both embryonal and postnatal periods of development. Distinct increase in lipoperoxidation was detected under conditions of chronic alcohol intoxication.
View Article and Find Full Text PDFExperiments involving chronic introduction of ethanol (36 per cent of caloric value) as a part of a specially devised liquid ration demonstrated the trainability of rats to sharply decrease, their antistress resistance to significantly decline, especially in rats kept on a low-protein diet. A general tendency toward a reduced activity of acetylcholinesterase in different sectors of the brain was revealed both in animals receiving alcohol against the background of a normal protein allowance and in those kept on a low-protein diet (when compared with the enzyme activity in animals maintained on a ration with a normal of protein).
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