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MP8 Metals in the Environment: Dietary concerns in Aquatic Systems
(DRE-1117-277986) Increased ovarian follicular apoptosis in fathead minnows exposed to dietary methylmercury.
Drevnick, P1, Sandheinrich, M2, Oris, J1, 1 Department of Zoology, Miami University, Oxford, OH, USA2 Department of Biology, University of Wisconsin-La Crosse, La Crosse, Wi, USA
ABSTRACT- Exposure to environmentally relevant concentrations of dietary methylmercury reduces the reproductive success of fish. The specific mechanism for this is unknown. However, recent research has linked altered reproduction in fish to the suppression of sex hormones by methylmercury. We hypothesize that methylmercury increases gonadal cell apoptosis in fish, thereby reducing the cell population available for synthesis of sex 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 (control), 0.87 (low), 3.93 (medium) g Hg/g dry weight. Apoptosis was evaluated histologically in ovaries of female fathead minnows by terminal deoxynucleotidyl transferase-mediated deoxyUTP nick end labeling (TUNEL). Methylmercury significantly increased the number of apoptotic follicular cells in stage III and IV oocytes. Increased ovarian follicular apoptosis was also related to suppressed 17-estradiol concentrations and smaller ovary size of female fathead minnows. Our results suggest increased gonadal cell apoptosis as a possible mechanism for the suppression of sex hormones and ultimately the reduction of reproductive success in fish exposed to methylmercury.
Key words: methylmercury, apoptosis, reproduction, fathead minnow
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