Abstract
Hypoxia has a profound effect on fish reproduction and development. Behavioral studies revealed that hypoxia can affect courtship behaviors, mate choice, and reproductive efforts in fish. Both laboratory and field evidence showed that hypoxia can cause major reproductive impairments by inhibiting testicular and ovarian development, affecting production and quality of sperm and egg, reducing fertilization and hatching success, and affecting larval survivorship as well as the quality and fitness of juveniles. Emerging evidence further showed that hypoxia does not impair these key reproductive processes through a general down‐regulation of metabolism and reproductive functions, but does so by affecting specific hormones, neurotransmitters, and receptors along the hypothalamus–pituitary–gonad axis as well as certain enzymes controlling steroidogenesis and vitellogenesis. In zebrafish, hypoxia has been shown to down‐regulate CYP19 and alter the ratio of testosterone to estradiol during early sex development, leading to a male‐biased F1 generation.
Hypoxia has been shown to delay embryonic development and hatching in many fish species, and embryos in some species may undergo complete developmental arrest under anoxia. In zebrafish embryos, blastomeres were arrested during the S and G2 phases of the cell cycle under anoxia. Fish embryos developed under hypoxia lost their normal synchronization, and abnormalities in spinal and vascular development are commonly observed. Results of both laboratory and field studies showed a higher percentage of malformation in fish developed under hypoxic conditions, possibly through altering their normal apoptosis.
Both in vitro and in vivo studies demonstrated that expression levels of certain genes directly or indirectly related to cell cycle, cell proliferation, and apoptosis, which underpin some of the fundamental processes related to development, are affected by hypoxia. Whether hypoxic inducible factor is involved in mediating the changes in gene expression and the observed reproductive and development impairments remains unclear. Copyright © 2009 Elsevier Inc. All rights reserved.
Hypoxia has been shown to delay embryonic development and hatching in many fish species, and embryos in some species may undergo complete developmental arrest under anoxia. In zebrafish embryos, blastomeres were arrested during the S and G2 phases of the cell cycle under anoxia. Fish embryos developed under hypoxia lost their normal synchronization, and abnormalities in spinal and vascular development are commonly observed. Results of both laboratory and field studies showed a higher percentage of malformation in fish developed under hypoxic conditions, possibly through altering their normal apoptosis.
Both in vitro and in vivo studies demonstrated that expression levels of certain genes directly or indirectly related to cell cycle, cell proliferation, and apoptosis, which underpin some of the fundamental processes related to development, are affected by hypoxia. Whether hypoxic inducible factor is involved in mediating the changes in gene expression and the observed reproductive and development impairments remains unclear. Copyright © 2009 Elsevier Inc. All rights reserved.
Original language | English |
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Pages (from-to) | 79-141 |
Journal | Fish Physiology |
Volume | 27 |
DOIs | |
Publication status | Published - 2009 |