TY - JOUR
T1 - Hypoxia to the skeletal systems of teleost
T2 - Impacts, mechanisms, and health implications
AU - Mo, Jiezhang
AU - Chen, Yinhua
AU - Lai, Keng Po
AU - Zhang, Zonghang
AU - Seemann, Frauke
AU - Liu, Wenhua
N1 - Publisher Copyright:
© 2025 Elsevier Ltd
PY - 2025/9
Y1 - 2025/9
N2 - Eutrophication, organic pollution, and climate change have fueled the frequency and extent of hypoxia in global aquatic ecosystems. Severe hypoxia in water bodies often results in mass mortality of aquatic organisms, a decline in fish populations, elimination of sensitive species. Hypoxia poses a significant threat to Darwinian fitness traits especially growth and reproductive capacities. While most studies focused on impacts of hypoxia on behaviors, development, and reproduction of fish, relatively few studies investigated the effects of hypoxia on skeletal systems. Notably, moderate hypoxia can induce skeletal deformities during embryonic and larval stages of fish, thereby affecting their locomotion, predator avoidance, inter- and intra-specific competition, and mating, which ultimately may affect population sustainability. The adverse impacts of hypoxia on fish skeletal system may be long-term and persist for multiple generations, warranting an updated systematic evaluation. This review summarizes the current knowledge of the impacts of hypoxia on the fish skeletal system, ranging from genetic and epigenetic mechanisms to multigenerational effects and potential health implications. Knowledge gaps are identified, and multigenerational research is proposed to assess bone integrity and fish health at epigenetic, molecular, proteomic, cellular, tissue, organismal, and population levels using model transgenic fish and wild fish. The critical dissolved oxygen level required for the induction of bone deformities and the underlying genetic and epigenetic mechanisms can serve as a guideline for assessing the health risks of hypoxia to fish for conservation and management purposes.
AB - Eutrophication, organic pollution, and climate change have fueled the frequency and extent of hypoxia in global aquatic ecosystems. Severe hypoxia in water bodies often results in mass mortality of aquatic organisms, a decline in fish populations, elimination of sensitive species. Hypoxia poses a significant threat to Darwinian fitness traits especially growth and reproductive capacities. While most studies focused on impacts of hypoxia on behaviors, development, and reproduction of fish, relatively few studies investigated the effects of hypoxia on skeletal systems. Notably, moderate hypoxia can induce skeletal deformities during embryonic and larval stages of fish, thereby affecting their locomotion, predator avoidance, inter- and intra-specific competition, and mating, which ultimately may affect population sustainability. The adverse impacts of hypoxia on fish skeletal system may be long-term and persist for multiple generations, warranting an updated systematic evaluation. This review summarizes the current knowledge of the impacts of hypoxia on the fish skeletal system, ranging from genetic and epigenetic mechanisms to multigenerational effects and potential health implications. Knowledge gaps are identified, and multigenerational research is proposed to assess bone integrity and fish health at epigenetic, molecular, proteomic, cellular, tissue, organismal, and population levels using model transgenic fish and wild fish. The critical dissolved oxygen level required for the induction of bone deformities and the underlying genetic and epigenetic mechanisms can serve as a guideline for assessing the health risks of hypoxia to fish for conservation and management purposes.
KW - Adverse effects
KW - Aquatic hypoxia
KW - Fish bone health
KW - Molecular mechanisms
KW - Risk assessment
UR - https://www.scopus.com/pages/publications/105009899644
U2 - 10.1016/j.jenvman.2025.126530
DO - 10.1016/j.jenvman.2025.126530
M3 - Review article
AN - SCOPUS:105009899644
SN - 0301-4797
VL - 391
JO - Journal of Environmental Management
JF - Journal of Environmental Management
M1 - 126530
ER -