2,3,7,8-Tetrachlorodibenzo-p-dioxin (
TCDD) has been shown to impair reproductive function of males in animal models, possibly due to a reduction in serum
androgen levels. Thus,
TCDD may alter the
testosterone biosynthetic pathway in the testis or the conversion of
testosterone to 5alpha-dihydrotestosterone (DHT) in
androgen target tissues. Pregnant Sprague Dawley rats were gavaged with
TCDD (0, 0.2 or 1.0 microg/kg) on day 15 of gestation only.
TCDD caused a reduction in the
body weight gain of the dams in both dose groups and a significant reduction in litter size in the higher dose group. Litters delivered normally and
TCDD exposed male offspring grew at the same rate as controls. Males were sacrificed at 15, 30, 45, 60, 90 and 120 d of age. Steroidogenic
enzyme activities were determined in testicular microsomes and
androgen target tissue nuclear fractions. Serum
androgens were measured by radioimmunoassay (RIA). At 30 d of age, rats exposed to 1.0 microg/kg
TCDD exhibited lower 17-hydroxylase activity (P < 0.05) and lower caput-corpus epididymal weights (P < 0.05). At 45 d of age, the same treatment resulted in testicular 3beta-HSD, 17beta-HSD and 5alpha-reductase activities that were significantly greater (P < 0.05) but, conversely, serum
androgens were one quarter the values evident in controls (P < 0.05). At the other ages, no differences were observed in serum
androgens and, with the exception of lower 17beta-HSD activity at 90 d of age (P < 0.05), no other differences in testicular steroidogenic
enzyme activities were found. 5Alpha-reductase activities in the
androgen target tissues were also unchanged. Histological examination of testes showed that the spermatogenic profile was identical to controls at all ages.