Effect of cadmium chloride on secretion of 17β-estradiol by the ovarian follicles of common carp, Cyprinus carpio

Cadmium (Cd2+) is a common environmental pollutant present in wastes associated with mining, smelting and electroplating. It is a major constituent of the tobacco smoke. Exposure of this heavy metal has been linked to wide range of detrimental effects on mammalian reproduction particularly on ovarian steroidogenesis. Low doses of Cd2+ are reported to stimulate ovarian luteal progesterone synthesis whereas high doses inhibited it. Cd2+ exposure is also reported to inhibit gonadal function in fish. In the present study the effects of cadmium chloride (CdCl2) on the secretion of gonadotropin-induced 17β-estradiol was examined in female common carp Cyprinus carpio. Vitellogenic stage fish were exposed to physiological safe dose of CdCl2 for 0, 24, 48 and 96 h and serum and ovarian 17β-estradiol levels were estimated. In the in vitro experiments, vitellogenic follicles were incubated with CdCl2 and a dose- and time-dependent effects on steroid production were estimated induced by LH. Exposure of fish with CdCl2 gradually attenuated serum and ovarian 17β-estradiol levels with increasing time and maximum inhibition was noticed after 96 h. Administration of CdCl2 to the incubations significantly inhibited LH-induced release of 17β-estradiol in vitro. To clarify the mechanism of attenuated production of 17β-estradiol, in vitro effects of CdCl2 on LH induced P450 aromatase activity (conversion of testosterone to 17β-estradiol) and cytochrome P450arom gene expression in carp ovarian follicles were evaluated. Results show that LH-stimulated P450 aromatase activity and P450arom gene expression in ovarian follicles were significantly inhibited by CdCl2. The present study further demonstrated that LH-induced stimulation of ovarian steroidogenic factor-1 (SF-1) which activates aromatase enzyme, is strongly inhibited by cadmium chloride treatment.

► In vivo exposure of C. carpio to CdCl2 attenuated serum and ovarian estradiol level.
► In vitro exposure of ovarian follicles to CdCl2 inhibited LH-induced E2 release.
► CdCl2 attenuated LH-stimulated P450aromatase activity in ovarian follicles.
► In vitro exposure to CdCl2 inhibited LH-stimulated ovarian P450arom gene expression.
► LH-induced stimulation of ovarian SF-1 was strongly inhibited by CdCl2.