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.

Suppressed adrenocortical responses and thyroid hormone levels in birds near a mercury-contaminated river.

Much of the research on sublethal, adverse effects of mercury (Hg) has focused on impairment of neurological function and reproduction in fish and fish-eating vertebrates. Here we examined the associations between Hg and endocrine function (adrenocortical responses and plasma thyroid hormone concentrations) of insectivorous tree swallow nestlings adjacent to a Hg-contaminated river and nearby reference rivers in Virginia. Nestlings from the contaminated sites had blood Hg concentrations that exceeded those from the reference sites by more than an order of magnitude (354 +/- 22 vs 17 +/- 1 ppb wet weight).

Perchlorate exposure induces hypothyroidism and affects thyroid-responsive genes in liver but not brain of quail chicks.

Ground-dwelling birds in perchlorate-contaminated areas are exposed to perchlorate ion, a known thyroid disruptor, and might be vulnerable to the developmental effects of perchlorate-induced hypothyroidism. We hypothesized that perchlorate-induced hypothyroidism would alter the expression of thyroid-responsive genes involved in thyroid hormone (TH) regulation and in the development of target organ function. Japanese quail chicks were exposed to 2000 mg/L ammonium perchlorate in drinking water for 7.

Effects of maternal exposure to ammonium perchlorate on thyroid function and the expression of thyroid-responsive genes in Japanese quail embryos.

Perchlorate, a known thyroid disruptor, is deposited in eggs of exposed female birds, raising concerns that the embryos from these eggs may become hypothyroid, which may in turn affect the development and function of thyroid-dependent organs. We hypothesized that exposure to ammonium perchlorate (AP) would decrease hen and embryonic thyroid function and affect the expression of thyroid-responsive genes in embryonic brain and liver. Laying Japanese quail hens were treated with 2000 mg/l or 4000 mg/l AP in drinking water.

Polychlorinated biphenyl effects on avian hepatic enzyme induction and thyroid function.

Polychlorinated biphenyls (PCBs) decrease thyroid function in laboratory rodents by inducing activity of a liver enzyme, uridine diphosphate-glucuronosyltransferase (UDP-GT), thereby increasing thyroxine (T4) clearance. This loss of T4 can lead to hypothyroidism. In this study, an assay was validated for measuring UDP-GT activity toward T4 in Japanese quail.