Effects of monocrotophos on the reproductive axis in the male goldfish (Carassius auratus): Potential mechanisms underlying vitellogenin induction

Monocrotophos (MCP) is a highly toxic organophosphorus pesticide that has been banned in many countries. Both vitellogenin mRNA expression and secretion were significantly induced in male goldfish by exposure to an MCP-based pesticide, suggesting that MCP has significant estrogenic properties. To elucidate the mechanisms of action of MCP on vitellogenin induction, we used radioimmunoassay to examine the effect of MCP treatment on plasma 17β-estradiol and testosterone levels in male goldfish (Carassius auratus). We also investigated the potential impacts of MCP treatment on aromatase expression, on the synthesis and secretion of pituitary gonadotropins and on the regulation of hypothalamic gonadotropin-releasing hormones by real-time PCR and radioimmunoassay. Experiments were carried out during the period of gonadal late recrudescence following a 21-day exposure to 0.01, 0.10 and 1.00 mg L−1 of a pesticide containing 40% MCP in a semi-static exposure system. The results indicated that males in each MCP treatment group had much higher plasma levels of 17β-estradiol, suggesting that the induction of VTG production by MCP was indirectly caused by elevated levels of endogenous 17β-estradiol. MCP-induced plasma 17β-estradiol levels via interference with the reproductive axis at multiple potential sites in male goldfish: (a) MCP exposure enhanced the mRNA expression of gonadal aromatase, the enzyme that converts androgens into estrogens, consequently reducing plasma levels of testosterone and increasing plasma concentrations of 17β-estradiol; (b) MCP treatment increased follicle-stimulating hormone β subunit mRNA expression and protein secretion and decreased luteinizing hormone β subunit mRNA expression and protein secretion, thus interfering with gonadotropin synthesis and secretion at the pituitary level and leading to the disruption of reproductive endocrine control and androgen and estrogen balance.