Abstract

Environmental contaminants with estrogenic activity have recently received attention because of their potential effects on the reproductive efficiency of humans and wildlife. This study was conducted with the endogenous estrogen, 17 β-estradiol (E2), to establish the histologic response of the fathead minnow ( Pimephales promelas) as a model organism. Sexually mature fathead minnows were exposed for 14 days to waterborne concentrations of 1000, 100, 10, 2, 1, 0.5, 0.25, 0.125, 0.1 or 0.0625 nM E2. Exposure to E2 caused a reduction in size of the prominent male secondary sex characteristics, the fatpads and nuptial breeding tubercles. Histological lesions observed in the testes included proliferation of Sertoli cells and degenerative changes. Electron microscopy of seminiferous tubules and their Sertoli cells revealed large phagolysosomes filled with degenerating spermatozoa and other cellular debris. Females had ovaries in which most of the follicles were in the primary stage of development. There were also more atretic follicles and fewer secondary and Graafian follicles than in unexposed females. These findings demonstrate components of sexually mature fish which may be altered by compounds that mimic E2. To determine if lesions observed in males were permanent, 50 sexually mature males and females were exposed to a single concentration of 10 nM E2 for 10 days. Samples were collected from males on the final day of E2 exposure and over a period of 16 weeks after the exposure was stopped. No E2-induced lesions were observed beyond 16 weeks post E2 exposure. Results of these studies suggest that histological lesions could occur at ecologically-relevant exposures to ‘estrogenic’ compounds. However, certain lesions caused by exposure of adult fathead minnows are not permanent.

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