Gordon G G, Vittek J, Ho R, Rosenthal W S, Southren A L, Lieber C S
Gastroenterology. 1979 Jul;77(1):110-4.
Hepatic testosterone 5-alpha-A-ring reductase (HTAR) activity was measured in open liver biopsies in eight alcohol-fed baboons and eight pair-fed controls. The animals were studied after at least 1 yr of alcohol feeding. In the alcholol-fed animals, a significant fall in enzyme activity was noted. This occurred whether the enzyme levels were related to soluble protein, to DNA, or to wet tissue weight, showing that the change was due to a decrease in the specific activity of the enzyme. In addition, aspiration liver biopsy specimens were obtained from 14 men and women with alcoholic liver disease. Again, there was a significant decrease in HTAH activity in these patients compared with a normal population. No relationship was found between hepatic histology and HTAR levels in either the baboon or human population with alcoholic liver disease, suggesting that the changes in enzyme activity were related to an alcohol effect rather than to liver disease per se. This study demonstrates that chronic alcohol use decreases the function of the enzyme which controls an important rate-limiting step in the metabolism of testosterone in the liver and that this effect may be due primarily to alcohol.
在八只喂食酒精的狒狒和八只配对喂食的对照动物的开放性肝活检中测量了肝脏睾酮5-α-A环还原酶（HTAR）活性。这些动物在至少一年的酒精喂养后接受研究。在喂食酒精的动物中，观察到酶活性显著下降。无论酶水平与可溶性蛋白、DNA还是湿组织重量相关，这种情况都会发生，表明这种变化是由于酶的比活性降低所致。此外，从14名患有酒精性肝病的男性和女性中获取了经抽吸的肝活检标本。同样，与正常人群相比，这些患者的HTAH活性显著降低。在患有酒精性肝病的狒狒或人群中，未发现肝脏组织学与HTAR水平之间存在关联，这表明酶活性的变化与酒精效应有关，而非与肝病本身有关。这项研究表明，长期饮酒会降低控制肝脏中睾酮代谢重要限速步骤的酶的功能，并且这种效应可能主要归因于酒精。
