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.
Hypoxia occurs over large areas in aquatic systems worldwide, and there is growing concern that hypoxia may affect aquatic animals, leading to population decline and changes in community by elimination of sensitive species. For the first time, we report that sublethal levels of hypoxia can significantly increase (+77.4%) malformation in fish embryonic development. Disruption of apoptotic pattern was clearly evident at 24 h post-fertilization, which may be a major cause of malformation. Furthermore, embryonic development was delayed, and balance of sex hormones (testosterone and estradiol) was disturbed during embryonic stages, implicating that subsequent sexual development may also be affected. Overall, our results imply that hypoxia may have a teratogenic effect on fish and delay fish embryonic development, which may subsequently impair species fitness leading to natural population decline.
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