Acetaldehyde directly inhibits the conversion of androstenedione to testosterone in the testes.
The effects of ethanol and acetaldehyde on testicular steroidogenesis were examined in enzymatically dispersed cells of the rodent testes. We found that both compounds significantly inhibited the gonadotropin-stimulated biosynthesis of testosterone. Acetaldehyde was approximately 4000 times more potent than its parent compound, however. Moreover, in contrast to the effects of ethanol, acetaldehyde was effective at concentrations compatible with those found under in vivo conditions after acute ethanol administration. These data indicate that acetaldehyde is, at the least, probably an extremely important factor in the well-documented ethanol-induced inhibition of testicular steroidogenesis in vivo and further suggest that ethanol may be converted to acetaldehyde to produce its testicular toxicity. Finally, we have found that acetaldehyde blocks testicular steroidogenesis by selectively and specifically inhibiting the conversion of androstenedione to testosterone.
D000079:Acetaldehyde / Q000494:pharmacology*; D000735:Androstenedione / Q000378:metabolism*; D000818:Animals; D001711:Biotransformation; D000431:Ethanol / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D011284:Pregnenolone / Q000494:pharmacology; D011374:Progesterone / Q000378:metabolism; D051381:Rats; D013737:Testis / Q000187:drug effects / Q000378:metabolism*; D013739:Testosterone / Q000096:biosynthesis*
D000431:Ethanol; D013739:Testosterone; D000735:Androstenedione; D011374:Progesterone; D011284:Pregnenolone; D000079:Acetaldehyde