Cadmium chloride-induced disruption of testicular steroidogenesis in rainbow trout, Oncorhynchus mykiss

Cadmium (Cd) is a known endocrine disruptor with the ability to affect the production of hormones involved in the regulation of reproductive processes. In the present study, the effects of CdCl(2) on unstimulated and stimulated testicular steroidogenesis were examined with the intention of furthering the understanding of the potential site(s) of action in the signaling pathway for 11-KT synthesis in teleosts. In short-term (2-h) exposures, CdCl(2) stimulated 11-KT production (29% and 28% over controls) in minced testicular tissues at concentrations of 10 and 100 mu M, respectively. However, 11-KT production was significantly lower than in controls (54%, 62%, and 54%) when tissues were incubated for 18 h with 1, 10, and 100 mu M Cd. Incubation of testicular tissues with 100 IU/ml human chorionic gonadotropin (hCG) and 5 mM dibutyryl-cAMP (dbcAMP), which activate rate-limiting steps in steroid synthesis, or 1.3 mu M 25-hydroxycholesterol (25-OHC), which augments production, resulted in significant increases in steroidogenesis over controls. hCG-stimulated steroidogenesis was reduced to 54% and 62% that of stimulated controls when tissues were incubated with CdCl(2) at 1 and 10 mu M, respectively. 11-KT production in dbcAMP-stimulated and 25-OHC-augmented tissues was not affected by Cd exposure. The results of this study indicate that one site of action of Cd in the signaling steroidogenic pathway is located prior to cAMP formation. This impairment could be overcome when higher concentrations of Cd were used in hCG-stimulated cells, suggesting the presence of a stimulatory site at, or following, hCG receptor binding.