Mercury-induced reproductive impairment in fish.

Mercury is a potent neurotoxin, and increasing levels have led to concern for human and wildlife health in many regions of the world. During the past three decades, studies in fish have examined the effects of sublethal mercury exposure on a range of endpoints within the reproductive axis. Mercury studies have varied from highly concentrated aqueous exposures to ecologically relevant dietary exposures using levels comparable to those currently found in the environment. This review summarizes data from both laboratory and field studies supporting the hypothesis that mercury in the aquatic environment impacts the reproductive health of fish. The evidence presented suggests that the inhibitory effects of mercury on reproduction occur at multiple sites within the reproductive axis, including the hypothalamus, pituitary, and gonads. Accumulation of mercury in the fish brain has resulted in reduced neurosecretory material, hypothalamic neuron degeneration, and alterations in parameters of monoaminergic neurotransmission. At the level of the pituitary, mercury exposure has reduced and/or inactivated gonadotropin-secreting cells. Finally, studies have examined the effects of mercury on the reproductive organs and demonstrated a range of effects, including reductions in gonad size, circulating reproductive steroids, gamete production, and spawning success. Despite some variation between studies, there appears to be sufficient evidence from laboratory studies to link exposure to mercury with reproductive impairment in many fish species. Currently, the mechanisms underlying these effects are unknown; however, several physiological and cellular mechanisms are proposed within this review.

Hormone cross-regulation in the tadpole brain: developmental expression profiles and effect of T3 exposure on thyroid hormone- and estrogen-responsive genes in Rana pipiens.

During metamorphosis, the tadpole neuroendocrine brain is a major target for the organisational effects of hormones acting via both endocrine feedback mechanisms and local hormone production. While the receptor-mediated actions of thyroid hormones in brain development have been well described, there is evidence that thyroid hormones could also be an important modulator of estrogen action during metamorphosis. To better understand hormone action and potential cross-regulation between thyroid hormone and estrogen, we examined changes in thyroid hormone receptors (TRalpha and TRbeta) and the estrogen receptor (ERalpha) in the brain of Rana pipiens throughout metamorphosis and in response to 48 h waterborne triiodothyronine (T3) exposure (0.5, 5 and 50 nM). We also measured mRNA levels of iodothyronine deiodinase (D2 and D3) and aromatase, key enzymes responsible for local synthesis and availability of thyroid hormones and estrogen, respectively. A real-time PCR strategy targeting these genes was developed using either a fluorescent dual-labelled probe- or SYBR Green I-based method. TRbeta mRNA levels were increased during development and in response to T3 exposure. Deiodinase (D2 and D3) enzymes were differentially regulated during development, but mRNA levels of both were increased with 50 nM T3 exposure. ERalpha and aromatase mRNA levels significantly increased at metamorphic climax, but whereas estrogen receptor alpha mRNA levels were increased by 50 nM T3, aromatase mRNA levels were decreased. These results (1) demonstrate that the developing amphibian brain is an important site for stage-specific thyroid hormone regulation of nuclear receptors and hormone synthesis enzymes and (2) provide the basis for further studies exploring the physiological and functional significance of the cross-regulation between thyroid status and estrogen-sensitive genes in the brain during amphibian metamorphosis.