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Abstract

Pharmaceutical androgens and estrogens discharged into the aquatic environment are now known to induce adverse effects in fish and are a health concern for wildlife. Mosquitofish (Gambusia affinis) exposed to a pharmaceutical androgen, trenbolone, used to enhance cattle growth and found to pollute waters below feedlots in the USA, has been shown to alter the development of the anal fin of the females and disrupt gonopodium development in fry. In our work, we showed that altered gonopodium development was associated with disruption in the normal patterns of expression of 2 cloned androgen receptors. Furthermore, exposure to trenbolone at 1 µg/L induced spermatocytes in the ovary of sexually mature females. Roach (Rutilus rutilus) living in UK rivers are exposed to estrogenic chemicals in effluents derived from sewage treatment works and this causes feminizing effects, including the development of oocytes in the testis of males. The contraceptive estrogen ethinylestradiol (EE2) is believed to contribute to these feminized responses. Our lab-based studies showed that gonadal feminization of roach could be induced by exposure to EE2 at 4 ng/L and the phenotypic responses were associated with altered patterns of expression of 2 cloned estrogen receptors (ERs) and aromatase genes. EE2 was shown to induce similar feminized responses in the medaka (Oryzias latipes). We established a reporter gene assay system for roach and medaka ERs and showed that specific environmental estrogens differentially activated the two fish ER subtypes. We also found evidence for an enhanced sensitivity for some estrogens to activate the medaka ERs compared with the roach ERs.

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