Increased ovarian follicular apoptosis in fathead minnows (Pimephales promelas) exposed to dietary methylmercury.

Exposure to environmentally relevant concentrations of dietary methylmercury impairs the reproduction of fish. Although specific mechanisms are unknown, recent research has linked altered reproduction in fish to the suppression of circulating levels of sex steroid hormones by methylmercury. We hypothesize that methylmercury induces apoptosis in steroidogenic gonadal cells in fish, thereby interfering with the synthesis of sex steroid hormones critical for the regulation of reproduction. To test this hypothesis, we chronically exposed fathead minnows (Pimephales promelas) to one of three diets contaminated with methylmercury: 0.06 microg Hg g(-1) (control), 0.87 microg Hg g(-1), and 3.93 microg Hg g(-1) dry weight. Apoptosis was evaluated histologically in ovaries of female fathead minnows by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL). Methylmercury significantly increased the number of apoptotic follicular cells in primary growth and cortical alveolus stage ovarian follicles. Ovarian follicular cells (i.e., granulosa, theca) are responsible for the production of 17beta-estradiol and other sex steroid hormones. Increased ovarian follicular apoptosis was related to suppressed 17beta-estradiol concentrations and smaller ovary size of female fathead minnows. Our results suggest increased apoptosis of steroidogenic gonadal cells as a possible mechanism for the suppression of sex steroid hormones and ultimately the impairment of reproduction in fish exposed to methylmercury.