TY - JOUR
T1 - The effects of maternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin on testicular steroidogenesis in infantile male rats
AU - Haavisto, T. E.
AU - Myllymaki, S. A.
AU - Adamsson, N. A.
AU - Brokken, L. J.
AU - Viluksela, M.
AU - Toppari, J.
AU - Paranko, J.
N1 - Haavisto, T E Myllymaki, S A Adamsson, N A Brokken, L J S Viluksela, M Toppari, J Paranko, J eng Research Support, Non-U.S. Gov't England Int J Androl. 2006 Apr;29(2):313-22. doi: 10.1111/j.1365-2605.2005.00568.x.
PY - 2006
Y1 - 2006
N2 - Exposure of adult male animals to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) decreases serum androgen concentrations. Reduction in androgen levels after maternal exposure has also been reported, but these results have not been reproduced. We have earlier shown that TCDD stimulates rather than inhibits testosterone synthesis in the prenatal rat testis. The aim of the present study was to elucidate in utero-induced effects of TCDD on testicular steroidogenesis in the 14-day-old infant rats. At that time the foetal Leydig cell population is still the prevailing source of androgens. Pregnant Sprague–Dawley dams were given a single oral dose of TCDD (0, 0.04, 0.2, or 1.0 μg/kg) on day 13 of pregnancy. On postnatal day 14, the body weight of male offspring was reduced after exposure to 1.0 μg/kg TCDD (from 33.9 ± 1.66 g to 31.6 ± 2.67 g). Relative testis weight, plasma testosterone, luteinizing hormone and follicle-stimulating hormone levels remained unaltered in all exposure groups. Moreover, in ex vivo incubations, testosterone and cAMP production was not affected. StAR protein level in the freshly isolated testes was increased in the 0.2 μg/kg group, and seminiferous cord diameter in the 0.04 μg/kg group. The present study confirms our earlier findings in in utero TCDD-exposed foetal testis indicating that maternal TCDD exposure does not negatively influence the developmental testosterone production of foetal type Leydig cells in rats.
AB - Exposure of adult male animals to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) decreases serum androgen concentrations. Reduction in androgen levels after maternal exposure has also been reported, but these results have not been reproduced. We have earlier shown that TCDD stimulates rather than inhibits testosterone synthesis in the prenatal rat testis. The aim of the present study was to elucidate in utero-induced effects of TCDD on testicular steroidogenesis in the 14-day-old infant rats. At that time the foetal Leydig cell population is still the prevailing source of androgens. Pregnant Sprague–Dawley dams were given a single oral dose of TCDD (0, 0.04, 0.2, or 1.0 μg/kg) on day 13 of pregnancy. On postnatal day 14, the body weight of male offspring was reduced after exposure to 1.0 μg/kg TCDD (from 33.9 ± 1.66 g to 31.6 ± 2.67 g). Relative testis weight, plasma testosterone, luteinizing hormone and follicle-stimulating hormone levels remained unaltered in all exposure groups. Moreover, in ex vivo incubations, testosterone and cAMP production was not affected. StAR protein level in the freshly isolated testes was increased in the 0.2 μg/kg group, and seminiferous cord diameter in the 0.04 μg/kg group. The present study confirms our earlier findings in in utero TCDD-exposed foetal testis indicating that maternal TCDD exposure does not negatively influence the developmental testosterone production of foetal type Leydig cells in rats.
U2 - 10.1111/j.1365-2605.2005.00568.x
DO - 10.1111/j.1365-2605.2005.00568.x
M3 - Article
SN - 0105-6263
VL - 29
SP - 313
EP - 322
JO - International Journal of Andrology
JF - International Journal of Andrology
IS - 2
ER -
