The effects of endocrine disrupting chemicals on the sexual development of fish

Environmental pollutants are suspected of causing observed adverse effects on development and reproduction in fish and wildlife. Evidence from the laboratory and field suggests that low levels of synthetic or natural chemicals that modulate or disrupt endocrine processes may be responsible. The aquatic environment is a sink for most all potential endocrine disrupting chemicals (EDCs). From egg fertilization to spawning, fish may be exposed to complex mixtures of steroidogenic chemicals that can interfere with the important activational and organizational processes of their endogenous hormones. One consequence of exposure to EDCs may be disruption of the normal mechanisms of sexual development and differentiation, processes that are highly hormone dependent, with subsequent adverse effects on reproduction.; My experiments address the hypothesis that exposure to EDCs during early ontogeny affects sexual development and differentiation in fish manifest at maturation. The dr-R strain of medaka was used as the test organism because of qualities that make it a good laboratory animal model and because it possesses a sex-linked gene for body color allowing visual determination of genetic sex from hatch. Medaka were exposed in ovo by nano-injection to five chemical compounds known or suspected to be hormone mimics or disruptors. Details of the effects resulting from exposure to the synthetic sex steroids ethinyl estradiol (EE₂) and methyl testosterone (MT) provided a reference and established a model for predicting effects of in ovo exposure to chemicals which mimic estrogens and androgens. Effects on medaka exposed to the EDCs, o,p′-DDE and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and three mixtures of polychlorinated naphthalenes (PCN), which have not been tested for their endocrine disrupting potential, were also investigated.; In ovo exposure to 0.5 and 2.5 ng EE₂/embryo or 0.8 and 8.0 ng MT/embryo affected sexual differentiation by causing sex reversal in males and females, respectively. Sexual development of male and female gonads was also affected at these doses. Most notably, all doses of MT resulted in precocious maturation of male and female medaka. Effects on sexual differentiation of the gonads were not as apparent for o,p′ -DDE, TCDD, and the PCNs as were effects on sexual development. Observed effects of these chemicals included one or more abnormalities: histopathological lesions (e.g., atresia), reduced gonad size, and changes in primary germ cell numbers along with volume of primordial gonads. Results for these chemicals together with other's field and laboratory observations provide further evidence that environmental EDCs may be adversely affecting reproduction and development of wild fishes. These results also support the utility of laboratory studies with the dr-R medaka model within the framework of a weight-of-evidence approach to establish a cause-and-effect relationship between environmental exposure to EDCs and reproductive impairment at the individual and population levels.