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- W1529455781 abstract "Hypoxia survival requires a well-coordinated response to either secure more O2 from the depleted environment or to defend against the metabolic consequences of too little O2 at the mitochondria, which limits aerobic ATP production. Inhibition of aerobic ATP production during hypoxia exposure imposes a substrate-limited cap on the duration of survival because O2-independent ATP production (anaerobic) is far less efficient than aerobic ATP production. It has long been held that hypoxia-tolerant animals are able to extend the period of survival under severely hypoxic conditions through a depression of basal metabolic rate, which limits the extent of activation of O2-independent pathways of ATP production. This contention appears to be supported by the available literature; however, more studies measuring metabolic rate during hypoxia exposure are needed before a definitive outcome can be decided. Duration of hypoxia exposure is also an important component to consider when assessing the responses to hypoxia. Long-term hypoxia exposure (> a few hours in some cases) can result in large changes in gene expression, which underlie acclimation/acclimatization and potentially enhance hypoxic survival. Hypoxia-mediated changes in gene expression are likely regulated by the transcription factor, hypoxia inducible factor (HIF), which is well characterized in mammalian systems, but has only recently been examined in fish. Hypoxia inducible factor appears to be regulated in a similar fashion in fish as in mammals, but to date, there does not appear to be a direct link between HIF function and hypoxia tolerance in fish." @default.
- W1529455781 created "2016-06-24" @default.
- W1529455781 creator A5046304119 @default.
- W1529455781 date "2009-01-01" @default.
- W1529455781 modified "2023-10-16" @default.
- W1529455781 title "Chapter 10 Metabolic and Molecular Responses of Fish to Hypoxia" @default.
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- W1529455781 doi "https://doi.org/10.1016/s1546-5098(08)00010-1" @default.
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