5. Conclusions
We
identified a large number of hypoxia associated markers in the muscles
of P. vachelli that were involved in diverse biological pathways
such as HIF-1 signaling, energy metabolism, and muscle function.
Compared with the P. vachelli livers, we found that muscles
experienced significant hypoxia-associated changes, and this was evident
in discrete tissue-specific patterns present. For example, P.
vachelli livers have increased anaerobic glycolysis, heme synthesis,
erythropoiesis, and inhibited apoptosis when exposed to under 4 h of
hypoxia, whereas the opposite was true to muscles.
To maintain normal physical activity, fishes acutely react to acute
hypoxia, by activated catabolic pathways to generate more energy,
decreased biosynthesis to reduce energy consumption, and shifted from
aerobic to anaerobic metabolic contributions. We found that hypoxia
induced muscle dysfunction through impairing mitochondrial function,
activating inflammasome, and apoptosis
(Zhou et al. 2011). The
hypoxia-induced mitochondrial dysfunction enhanced ROS generation and
apoptosis, further triggering IL-1β production via the inflammasome
activation (Pomerantz et al.2001). In turn, IL-1β further impaired mitochondrial function and
apoptosis by suppressing downstream mitochondrial biosynthesis related
proteins, resulting in a vicious circle between inflammasome activation
and mitochondrial dysfunction (Yi et
al. 2015) (Fig. 7 ). We hope that it provides fundamental data
on analytical methods, as well as biological and mechanical insights
into future research for
environmental stress induced
hypoxia.