Centre for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, 20 Marie Curie, Ottawa, Ontario K1N 6N5, Canada.
Environ Toxicol Chem. 2010 Aug;29(8):1804-15. doi: 10.1002/etc.232.
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.
暴露于多种环境胁迫因子会对全球范围内的两栖动物健康产生负面影响。增加的紫外线 B 辐射(UVBR)和化学污染物的暴露可能通过干扰变态来影响两栖动物种群;然而,这些胁迫因子影响发育的实际机制尚不清楚。由于两栖动物的变态受甲状腺激素(TH)的控制,环境胁迫引起的发育率变化表明甲状腺系统受到干扰。在受到外源性 TH 三碘甲状腺原氨酸(T3;5 或 50 nM)的挑战之前,蝌蚪被慢性暴露于环境水平的 UVBR(平均 0.15 W/m2)和 4-叔辛基苯酚(OP;10 nM),单独和组合。这种实验方法是为了确定暴露于这些胁迫因子是否会影响 T3 引发特定分子和形态学反应的能力。OP 暴露增加了脑中甲状腺受体(TR)alpha 和 beta、脱碘酶 2(D2)和促肾上腺皮质激素释放激素以及尾部 D2 的 mRNA 水平。4-叔辛基苯酚还增强了 T3 在脑中诱导的 D2 表达。UVBR 和 OP 的组合影响了脑中 TR alpha 的表达以及尾部 TR alpha 和 beta 基因对 T3 的反应,表明考虑多种胁迫因子对两栖动物的影响非常重要。暴露于 UVBR 的蝌蚪发育延迟,并在暴露于 T3 后表现出尾部吸收速度减慢和后肢发育加速。总之,这些发现表明,UVBR 改变了变态时的发育速度和 TH 依赖性形态变化,并且暴露于 UVBR 和/或 OP 会破坏发育和 T3 在周围组织中的生物学作用的重要基因的表达。我们小组是第一个证明环境水平的 UVBR 和/或 OP 可以影响两栖动物甲状腺系统的小组。