There is increasing concern that certain chemicals in the aquatic environment can disrupt endocrine systems, leading to reproductive impairment and threatening survival of wild populations of invertebrates, fish, bird, reptiles, and wildlife. For the first time, we report that hypoxia is also an endocrine disruptor and poses a significant threat to the reproduction and hence sustainability of fish populations. Serum levels of testosterone, estradiol, and triiodothyronine significantly decreased in carp (Cyprinus carpio) upon chronic exposure to hypoxia. These hormonal changes were associated with retarded gonadal development in both male and female carp, reduced spawning success, sperm motility, fertilization success, hatching rate, and larval survival, indicating that adverse effects of hypoxia on reproductive performance resulted from endocrine disruption. Since aquatic hypoxia commonly occurs over thousands of square kilometers in aquatic systems worldwide, our results imply that endocrine disruption and reproductive impairment in fish may be a widespread environmental problem.

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Certain fish have the remarkable capability of euryhalinity, being able to withstand large variations in salinity for indefinite periods. Using the highly euryhaline species, silver sea bream (Sparus sarba), as an experimental model, some of the molecular processes involved during ion regulation (Na+-K+-ATPase), cytoprotection [heat shock protein (hsp) 70], and growth (somatotropic axis) were studied. To perform these studies, seven key genes involved in these processes were cloned, and the tissue-specific expression profiles in fish adapted to salinities of 6 parts per thousand (ppt; hypoosmotic), 12 ppt (isoosmotic), 33 ppt (seawater), and 50 ppt (hypersaline) were studied. In gills, the transcriptional and translational expression profiles of Na+-K+-ATPase alpha- and beta-subunit genes were lowest in isoosmotic-adapted fish, whereas in kidneys the expression of the beta-subunit increased in seawater- and hypersaline-adapted groups. The hsp70 multigene family, comprising genes coding for heat shock cognate (hsc70), inducible heat shock protein (hsp70), and a heat shock transcription factor (hsf1), was found to be highly upregulated in gills of seawater- and hypersaline-adapted fish. In liver, hsc70 expression was lowest in isoosmotic groups, and in kidneys the hsp70 multigene family remained unchanged over the salinity range tested. The regulation of the somatotropic axis was studied by measuring pituitary growth hormone expression and liver IGF-I expression in salinity-adapted fish. The expression amounts of both genes involved in the somatotropic axis were highest in fish maintained at an isoosmotic salinity. The results of this study provide new information on key molecular processes involved in euryhalinity of fish.

The focus of this review is on the importance and regulation of fish growth hormone (GH), during exposure to stress. Alterations in environmental salinity impose osmoregulatory stress on fish and upon exposure to increased salinities GH has been shown to be important in maintaining hypoosmoregulatory function. Whilst studies mainly on salmonids, demonstrate that GH essentially performs a role as a seawater adapting hormone a clear correlation of elevated GH with growth and isoosmotic salinity exposure has been identified from studies on sparids. Variations in water temperature have been shown to modulate fish GH with the overall consensus of highest levels of GH during the warmer seasons of the year, suggesting an important role for GH during the temperature acclimatization process, but whether this relates to growth is unclear. Environmentally important pollutants, including xenoestrogens and heavy metals have been shown to affect GH mediated mechanisms, in fish, possibly via interference with the GH receptor and/or GH transcription, whereas aquacultural related stressors such as handling, confinement/overcrowding and nutritional stress have also been shown to affect GH levels. In addition the impact of aquacultural related stressors can also predispose fish to disease leading to chronic suppression of GH. Finally, GH has been recently demonstrated to exert an anti-apoptotic effect in fish cells, when exposed to chemical stress, providing evidence that GH can also serve as a protective agent.