Eicosanoids play an important role in the regulation of the hypothalamic-pi
tuitary axis; less clear is their role in testicular steroidogenesis. To ev
aluate the involvement of cyclooxygenase metabolites, such as prostaglandin
s, in the regulation of human testicular steroidogenesis, we examined the e
ffects of a prostaglandin-blocker, aspirin, on plasma testosterone, pregnen
olone, progesterone, 17OH-progesterone, androstenedione, dehydroepiandroste
rone, and 17 beta-estradiol response to human chorionic gonadotropin (hCG)
in normal male volunteers in a placebo-controlled, single-blinded study. To
test the efficacy of aspirin, seminal prostaglandin E-2 levels were also d
etermined. hCG stimulation increased peripheral levels of testosterone, 17O
H-progesterone, androstenedione, dehydroepiandrosterone, and 17 beta-estrad
iol, without affecting circulating pregnenolone and progesterone values. As
pirin significantly lowered seminal prostaglandin E-2 levels, whereas it di
d not modify steroid concentrations not exposed to exogenous hCG. Moreover,
the drug significantly reduced the response of testosterone, 17OH-progeste
rone, androstenedione, and dehydroepiandrosterone to hCG, as assessed by th
e mean integrated area under the curve, whereas it did not influence 17 bet
a-estradiol response. In conclusion, aspirin treatment inhibits androgen re
sponse to chorionic gonadotropin stimulation in normal humans. The action o
f aspirin is probably mediated via an effective arachidonate cyclooxygenase
block.