Ellingboe J, Varanelli C C
Res Commun Chem Pathol Pharmacol. 1979 Apr;24(1):87-102.
Ethanol was found to suppress gonadotropin-stimulated testosterone biosynthesis in sexually mature male rats in vivo and in intact Leydig cells in vitro. A similar ethanol dose-response inhibition curve was also observed when either whole or homogenized cells were stimulated by dibutyryl cyclic AMP. In the presence of pharmacologically relevant ethanol concentrations, added NAD+ restored testosterone production to stimulated control levels. These results demonstrate a direct inhibitory effect of ethanol on testicular testosterone synthesis. The site of inhibition is primarily intracellular and the mechanism is probably through a decrease in the NAD+/NADH ratio caused by ethanol oxidation.
在体内的性成熟雄性大鼠以及体外完整的睾丸间质细胞中,发现乙醇可抑制促性腺激素刺激的睾酮生物合成。当用二丁酰环磷腺苷刺激全细胞或匀浆细胞时,也观察到类似的乙醇剂量反应抑制曲线。在具有药理学相关性的乙醇浓度存在的情况下,添加烟酰胺腺嘌呤二核苷酸(NAD+)可使睾酮生成恢复到刺激对照组水平。这些结果表明乙醇对睾丸睾酮合成具有直接抑制作用。抑制位点主要在细胞内,其机制可能是乙醇氧化导致烟酰胺腺嘌呤二核苷酸/还原型烟酰胺腺嘌呤二核苷酸(NAD+/NADH)比值降低。