Rat fetuses from mothers stressed chronically by immobilization and high intensity illumination beginning on day 14 of gestation have higher than normal levels of Δ5-3β- hydroxysteroid dehydrogenase (3βHSD) activity in Leydig cells on day 17 of gestation and lower than normal levels on days 18 and 19. Plasma testosterone titers in normal and stressed male fetuses closely parallel the activity of 3βHSD in fetal Leydig cells. In the present study quantitative cytochemistry was used to determine whether the stress-induced alterations in 3βHSD activity could be prevented by treating the mother with naltrex-one, an opioid receptor blocker, before each stress session. Nal-trexone normalized 3βHSD activity on days 18 and 19 of gesta-tion, suggesting that the stress-induced suppression involves the endogenous opioid system. In contrast, naltrexone did not pre-vent the elevation in enzyme activity seen on day 17 in stressed fetuses. The persistence of a stress-induced surge on day 17, in spite of naltrexone therapy, suggests that some nonopioid mech-anism is operational at that time.
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