Borodkin Iu S, Bokiĭ I V, Usatenko M S, Sokolovskaia N E, Petrova M A
Farmakol Toksikol. 1985 May-Jun;48(3):99-103.
Alcohol dehydrogenase activity (ADH; KP 1.1.1.1.) in blood serum of rats and rabbits is 1 and 2 orders of magnitude higher than in humans. In chronic alcoholics, blood ADN is activated with an increase in alcoholism standing. Twelve hours after acute alcoholic intoxication alcoholics and heavy drinkers manifest a significant reduction in blood ADH activity. Acute alcoholic intoxication does not influence blood ADH in men who do not abuse alcohol. Chronic exposure of rabbits to ethanol leads to a decrease in ADH activity in the liver and to its rise in the blood. ADH activation is observed only in those animals which demonstrate the signs of fatty and protein liver dystrophy. It is concluded that chronic exposure to ethanol does not induce ADH synthesis in the liver. The blood ADH content ascends as a results of an increase in ADH transport from hepatocytes to the bloodstream.
大鼠和家兔血清中的酒精脱氢酶活性(ADH;KP 1.1.1.1.)比人类高1至2个数量级。在慢性酗酒者中,随着酗酒时间的增加,血液中的ADN被激活。急性酒精中毒12小时后,酗酒者和大量饮酒者的血液ADH活性显著降低。急性酒精中毒对不酗酒男性的血液ADH没有影响。家兔长期接触乙醇会导致肝脏中ADH活性降低,而血液中ADH活性升高。仅在那些出现脂肪肝和蛋白质营养不良迹象的动物中观察到ADH激活。结论是,长期接触乙醇不会诱导肝脏中ADH的合成。血液中ADH含量的升高是由于ADH从肝细胞向血液中的转运增加所致。