Dietary mercury has no observable effects on thyroid-mediated processes and fitness-related traits in wood frogs

Mercury (Hg) is a neurotoxicant known to cause developmental and behavioral abnormalities in vertebrates. Increasing evidence suggests that Hg can also disrupt endocrine functions and endocrine-dependent processes. For example, dietary Hg has been shown to delay tail resorption during metamorphic climax in amphibians, a process mediated by thyroid hormones. However, a direct link between Hg, hormone disruption, and developmental delays in amphibians has not been explored. Therefore, we examined the effects of dietary Hg (0.01, 2.5, and 10 μg/g total Hg, dry wt) on thyroid hormone concentrations, development, growth, performance, and survival of wood frogs (Rana sylvatica). Tadpoles accumulated Hg in a concentration-dependent manner; total Hg concentrations in tadpoles at the beginning of metamorphic climax (Gosner stage 42) were 0.03, 1.06, 3.54 μg/g, dry wt, for control, low, and high Hg diets, respectively. During metamorphic climax, tadpoles eliminated 35% of the inorganic Hg from their tissues but retained most of their accumulated methylmercury. Contrary to our predictions, we found no effect of Hg on the duration of tadpole development, size at metamorphosis, tail resorption time, or hopping performance. Consistent with the lack of effects on development, we also detected no differences in whole-body thyroid hormone concentrations among our dietary treatments. Our results, when compared with the effects of Hg on other amphibians, suggest that amphibian species may differ substantially in their sensitivity to dietary Hg, emphasizing the need for data on multiple species when establishing toxicity benchmarks.