Effects of embryonic exposure to androgen-active endocrine disrupting chemicals in Japanese quail

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2005-04-18

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Endocrine disrupting chemicals (EDCs) are compounds that alter the production, secretion, action, and elimination of endogenous hormones. EDCs have been shown to be responsible for disrupting development, reproduction, immune function, behavior, and all other life functions mediated by hormones. In the environment, organisms are exposed to many different types of EDCs at any one time, each with different mechanisms of action, many of which are not fully understood at present. Most research done with EDCs has focused on the effects of these chemicals on the estrogen and thyroid systems, however, many of these same chemicals also exert strong effects on the androgen system. Also, many studies assessing the effects of EDCs on wildlife have focused on reproductive measures of exposure, often overlooking potential effects on the immune system. We have demonstrated that embryonic exposure to androgen-active EDCs, anti-androgenic DDE and androgenic trenbolone acetate, impairs development of the bursa of Fabricius in Japanese quail, providing a possible mechanism for EDC-induced immunosuppression. The bursa is a primary immune organ responsible for development of the humoral part of the immune system. We have also demonstrated that the bursa can be resilient to embryonic exposure to EDCs, if post-hatch exposure to these chemicals is prevented. Measures of reproduction, behavior, growth, and developmental stability were also taken in this study. Male and female rates to sexual maturity were altered by the one-time in ovo exposure to DDE and trenbolone. Male reproductive behavior, as measured by attempts to mount and successful cloacal contacts achieved, was suppressed by both chemicals. Vocalization was abolished in one and two week old chicks from the highest trenbolone acetate treatment levels. Although environmentally relevant, the levels of DDE used in this study were below those reported to affects avian reproduction. Environmental levels of trenbolone acetate are unknown, however, previous studies have concluded trenbolone acetate to be safe to wildlife and non-teratogenic. The myriad of endpoints used in this study has been compiled to provide toxicologists with a list of sensitive and persistent measures that can be used as reliable biomarkers of exposure to androgen-active EDCs in birds.

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