Abstract
Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress
Weissman,Ben-Avi; Sottas,Chantal M.; Zhou,Ping; Iadecola,Costantino; Hardy,Matthew P.
American Journal of Physiology: Endocrinology and Metabolism (Translational Series) 292(2): E615-E620
Publication date: 2007
Immobilization stress (IMO) induces a rapid increase in glucocorticoidsecretion [in rodents, corticosterone CORT)] and this is associatedwith decreased circulating testosterone (T) levels. Nitric oxide(NO), a reactive free radical and neurotransmitter, has beenreported to be produced at higher rates in tissues such as brainduring stress. The biosynthesis of T is also known to be dramaticallysuppressed by NO. Specifically, the inducible isoform of nitricoxide synthase (iNOS) was directly implicated in this suppression.To assess the respective roles of CORT and NO in stress-mediatedinhibition of T production, adult wild-type (WT) and induciblenitric oxide synthase knockout (iNOS) male micewere evaluated. Animals of each genotype were assigned to eitherbasal control or 3-h IMO groups. Basal plasma and testicularT levels were equivalent in both genotypes, whereas testicularweights of mutant mice were significantly higher compared withWT animals. Exposure to 3-h IMO increased plasma CORT and decreasedT concentrations in mice of both genotypes. Testicular T levelswere also affected by stress in WT and mutant males, being sharplyreduced in both genotypes. However, the concentrations of nitriteand nitrate, the stable metabolites of NO measured in testicularextracts, did not differ between control and stressed WT andiNOS mice. These results support the hypothesisthat CORT, but not NO, is a plausible candidate to mediate rapidstress-induced suppression of Leydig cell steroidogenesis.
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