[Activity of the enzymes of ethanol and acetaldehyde metabolism in rats with varying initial sensitivity to alcohol]. / Aktivnost' fermentov metabolizma étanola i atsetal'degida u krys s razlichnoi iznachal'noi chuvstvitel'nost'iu k alkogoliu.

The experiments were carried out on male rats with different sensitivity to alcohol. To assess sensitivity to ethanol effects, we have used ethanol-induced sleep time and variations in rectal temperature of alcohol-intoxicated animals. Activity of alcohol dehydrogenase, microsomal ethanol-oxidizing system, catalase and aldehyde dehydrogenase in the liver as well as ethanol and acetaldehyde levels in the blood were determined after alcohol intoxication (3.5 g/kg, i.p., 8 days). The development of alcohol tolerance was accompanied by induction of the microsomal ethanol-oxidizing system in long-sleeping rats and in short-sleeping rats as well as by an increase in ethanol and acetaldehyde levels in the blood.

[Metabolic adaptation to alcohol in rats with different preference of ethanol over water]. / Metabolicheskaia adaptatsiia k alkogoliu u krys, razlichaiushchikhsia po predpochteniiu étanola vode.

Recent studies have shown that the phenomenon of ethanol preference by animals and of alcohol consumption by humans may be related to the intensity of its metabolism in the body and depend on the activities of the ethanol and aldehyde metabolizing systems which are potential regulators of the acetaldehyde level in the cell. The special features of adaptative reactions of this system (alcohol dehydrogenase, microsomal ethanol oxidizing system, catalase, aldehyde dehydrogenase) were examined in rats, differing by the preference to water or ethanol (5%, 10%, 15%) under condition of a long contact with alcohol.

[Effects of catalase activators and inhibitors on ethanol pharmacokinetic characteristics and ethanol and aldehyde-metabolizing enzyme activities in the rat liver and brain].

The effects of catalase regulators (aminotriazole, lead acetate, taurine, di-2-ethylhexylphthalate) on the preference for ethanol, its pharmacokinetics, and activities of rat liver and brain ethanol and acetaldehyde-metabolizing enzymes were studied. Lead acetate (100 mg/kg, i.p., 7 days), aminotriazole (1 g/kg, i.p., 7 days), and taurine (650 mg/kg, i.g., 14 days) decreased ethanol consumption under conditions of free choice (10% ethanol water), whereas di-2-ethylhexylphthalate (300 mg/kg, i.g., 7 days) did not exert any effect on this parameter. Taurine, lead acetate and di-2-ethylhexylphthalate significantly activated liver ADH, MEOS and catalase peroxidase activity. Aminotriazole also activated ADH and MEOS, but inhibited liver catalase. The activities of liver and brain A1DH as well as catalase were insignificantly changed by this treatment. The 7-day administration of lead acetate, di-2-ethylhexylphthalate and aminotriazole administrations significantly influenced the ethanol (2 g/kg., i.p.) pharmacokinetic parameters: the area under the pharmacokinetic curve and the elimination half-life time were significantly reduced, whereas the elimination constant and clearance were increased. This unequivocally indicates accelerated ethanol elimination. The 14-day ingestion of taurine insignificantly changed the parameters of ethanol pharmacokinetics in rats.

[Effect of acetaldehyde on ethanol- and aldehyde-metabolising systems of the liver and brain of rats]. / Vliianie atsetal'degida na étanol- i al'degidmetaboliziruiushchie sistemy pecheni i mozga krys.

Lately the mechanism of craving for alcohol has been related to the local level of brain acetaldehyde occurring in ethanol consumption and depending on the activities of the brain and liver ethanol and acetaldehyde-metabolizing systems. In this connection, we studied the effect of chronic acetaldehyde intoxication on the activities of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), the microsomal ethanol oxidizing system (MEOS) and liver and brain catalase as well as ethanol and acetaldehyde levels in the blood. The results showed that the chronic acetaldehyde intoxication did not alter significantly the activities of liver ADH, MEOS and catalase as well as liver and brain ALDH. In parallel with this, the systemic acetaldehyde administration led to shortened time of ethanol narcosis and activation of catalase in the cerebellum and left hemisphere, which may indicate involvement of this enzyme into metabolic tolerance development.