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Biomedical subjects

P P Voronov

Publications and source records attributed to P P Voronov.

8 recordsLinked to original sources

[Immunoenzyme and immunohistochemical analysis of class III alcohol dehydrogenase from human testis].

An enzyme-linked immunosorbent assay on the basis antialcohol dehydrogenase III (ADH III) monospecific antiserum has been devised. The immunoreactive protein content determined in two samples of human testis autopsy material was 1,288 and 1,047 mg/g of wet weight. ADH III has been revealed in all types of human testicular cells with the maximal content in spermatocytes and spermatogonia.

Alcohol Dehydrogenase↗

[Ethanol-metabolizing enzymes from human testis].

Testicular ethanol-metabolizing enzymes (alcohol dehydrogenase, microsomal ethanol-oxidizing system, catalase) were investigated. Alcohol dehydrogenase was purified to homogeneity and its main kinetic parameters were analyzed. It was shown that alcohol dehydrogenase corresponds to class III isozymes and does not participate in ethanol oxidation. The testicular microsomal ethanol-oxidizing activity does not exceed 0.02 nmol/min/mg of protein. The activity of catalase and its peroxidase component is far lower in the testes than in the liver. On the whole, testicular tissue is rather inactive in respect of ethanol oxidation.

Alcohol Dehydrogenase↗

[Corticosterone level in testes of rats in varying adrenal functional activity].

The presence of corticosterone in rat testes was demonstrated by combining HPLC and RIA techniques. The presence of the hormone was also taken into account. The testicular corticosterone content was shown to depend upon the functional activity of the adrenals and to diminish acutely after adrenalectomy. Analysis of correlation between the concentration of the hormones in the plasma and testes has shown corticosterone to be formed by testicular cells.

Adrenal Glands↗

[Nicotinamide has no effect on the ethanol-induced decrease in testosterone biosynthesis].

Administration of ethanol to Wistar rats in a dose of 3.5 g per 1 kg of the weight is accompanied by a decrease of testosterone concentration in the blood plasma. Nicotinamide, a NAD predecessor, exerts no effect on this index being applied in a dose of 200 mg/kg and does not modify the action of ethanol being administered in combination with the latter NAD concentration in the testicles as well as the rate of its utilization in the course of poly-ADP-ribose synthetase reaction remains unchanged. The data obtained contradict the hypothesis that ethanol effects in the testicles are determined by accessibility of oxidated NAD.

Animals↗

[Mechanism of suppression of testosterone biosynthesis by ethanol].

The paper is concerned with a study of the mechanism of ethanol induced testosterone biosynthesis inhibition in rat testis. The time course of acute alcoholic intoxication (4 g of ethanol per 1 kg of body mass) has shown that the size and direction of testosterone concentration shifts resemble those of corticosterone. The level of the latter correlates with the ethanol concentration rising at the early time of the experiment and lowering up to 26-27% in 4-8 h. The content of testis cyclic AMP, leu-enkephalin and beta-endorphin remains unchanged indicating against the hypothesis of ethanol effects mediation by the testicular opioid system.

Animals↗

[Effect of acute alcohol intoxication on lipid peroxidation in testis and adrenal glands of rats].

Hormones level and lipid peroxidation processes under influence of acute alcohol intoxication are tested in testes and adrenals of rats. Ethanol marker effects--the rise of corticosterone biosynthesis and depression of testosterone concentration--were reproduced in the experiment. At the moment of maximal changes in steroid levels indices characterising lipid peroxidation didn't differ from the control. At the early stage of the experiment transient shifts in malonic dialdehyde and dienic conjugates levels were noted. The data obtained does not agree with the hypothesis of acute ethanol effects in testes and adrenals being mediated through the changes of lipid peroxidation rate.

Adrenal Glands↗

[Influence of ethanol and ethanol-induced lipid peroxidation on the steroidogenic activity of testicles].

Chronic alcohol intoxication results in the diminished testosterone level and activation of lipid peroxidation in rat testes. A significant decrease in 3 beta-hydroxysteroid-hydrogenase and 17-dehydrogenase activity has been observed in microsomes. Analogous shifts have been evoked in vitro by the induction of lipid peroxidation in microsomes. That permitted one to suppose that alcohol-induced alterations in tests are partially mediated by induction of lipid peroxidation.

Alcoholism↗

[Effect of ethanol and lipid peroxidation on testosterone biosynthesis by interstitial cells of rat testes].

The induction of lipid peroxidation in interstitial cells of rat testes of ADP-Fe3+ complex results in the decrease of testosterone biosynthesis. Ethanol at 50 mM concentration enhances the level of malonic dialdehyde and inhibits the steroidogenesis. Effects of alcohol and ADP-Fe3+ complex both on lipid peroxidation or testosterone biosynthesis are additive. This agrees with the idea about the mediation of ethanol effects in testes by the induction of lipid peroxidation.

Adenosine Diphosphate↗