In vivo effects of stress, ACTH and corticosterone on testicular 11 beta-hydroxysteroid dehydrogenase oxidative activity in rats and the possible mechanism of actions

Citation
Khh. Nwe et al., In vivo effects of stress, ACTH and corticosterone on testicular 11 beta-hydroxysteroid dehydrogenase oxidative activity in rats and the possible mechanism of actions, EXP CL E D, 108(5), 2000, pp. 369-377
Citations number
34
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES
ISSN journal
09477349 → ACNP
Volume
108
Issue
5
Year of publication
2000
Pages
369 - 377
Database
ISI
SICI code
0947-7349(2000)108:5<369:IVEOSA>2.0.ZU;2-K
Abstract
The effects of stress and corticosterone on testicular 11 beta-hydroxystero id dehydrogenase (11 beta-HSD) oxidative activity have been controversial, whilst that of adrenocorticotrophic hormone (ACTH) have not been investigat ed before. Hence, the aim of the present study was to determine the in vivo effects of stress due to injection and sham operation, ACTH and corticoste rone on testicular and hepatic 11 beta-HSD oxidative activity and plasma te stosterone levels in normal and adrenalectomized (ADX) rats and their possi ble mechanism of actions. Adrenalectomy reduced both testicular 11 beta-HSD oxidative activity and plasma testosterone levels. The effects of injectio n and sham operation significantly increased plasma corticosterone levels w ith decreased testicular 11 beta-HSD oxidative activity and plasma testoste rone levels in normal but not in ADX rats. Likewise, ACTH or corticosterone treatment for 7 days decreased both testicular 11 beta-HSD oxidative activ ity in a dose dependent manner and plasma testosterone levels in normal rat s; but the values in ADX rats remained unchanged. However, none of the abov e values were significantly lower than that of the ADX levels. Corticostero ne seems to maintain testicular 11 beta-HSD oxidative activity within the r ange between normal and ADX rats. These changes are not attributable to diu rnal rhythms, as the time of sacrifice has been fixed between 8:30 and 10:3 0 am. In the liver, no significant change in 11 beta-HSD oxidative activity was observed with sham operation, ACTH or corticosterone treatment; but ad renalectomy significantly decreased it. In conclusion, in the intact normal rats, stress, ACTH or corticosterone modulates testicular (but not hepatic ) 11 beta-HSD oxidative activity indirectly through the adrenal glands and the physiological level of corticosterone is ideal for normal reproductive functions.