Exposure to multiple environmental stressors is negatively impacting the health of amphibians worldwide. Increased exposure to ultraviolet B radiation (UVBR) and chemical pollutants may affect amphibian populations by disrupting metamorphosis; however, the actual mechanisms by which these stressors affect development remain unknown. Because amphibian metamorphosis is controlled by thyroid hormones (TH), changes in developmental rates by environmental stress suggest a disruption of the thyroid system. Tadpoles were chronically exposed to environmental levels of UVBR (average of 0.15 W/m2) and 4-tert-octylphenol (OP; 10 nM), alone and combined, prior to being challenged to exogenous TH triiodothyronine (T3; 5 or 50 nM). This experimental approach was taken to determine whether exposure to these stressors affects the ability of T3 to elicit specific molecular and morphological responses. Exposure to OP increased mRNA levels of thyroid receptors (TRs) alpha and beta, deiodinase type 2 (D2), and corticotropin releasing hormone in the brain and of D2 in the tail of tadpoles. 4-tert-octylphenol also enhanced T3-induced expression of D2 in the brain. The combination of UVBR and OP affected the expression of TR alpha in the brain and the responses of TR alpha and beta genes to T3 in the tail, demonstrating the importance of considering the effects of multiple stressors on amphibians. Tadpoles exposed to UVBR were developmentally delayed and exhibited slowed tail resorption and accelerated hindlimb development following exposure to T3. Together, these findings indicate that UVBR alters the rate of development and TH-dependent morphological changes at metamorphosis, and that exposure to UVBR and/or OP disrupts the expression of genes important for development and the biological action of T3 in peripheral tissues. Our group is the first to demonstrate that environmental levels of UVBR and/or OP can affect the thyroid system of amphibians.
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