Nitric Oxide Drives Mitochondrial Energetics in Heart and Liver Mitochondria of Hypoxia-Stressed Climbing Perch (Anabas testudineus Bloch)
Authors
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Department of Zoology, School of Life Sciences, University of Kerala, Kariavattom, Thiruvananthapuram – 695581, Kerala ,IN
R. Gayathry -
Inter-University Centre for Evolutionary and Integrative Biology iCEIB, School of Life Sciences, University of Kerala, Kariavattom, Thiruvananthapuram – 695581, Kerala ,INValsa S. Peter
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Inter-University Centre for Evolutionary and Integrative Biology iCEIB, School of Life Sciences, University of Kerala, Kariavattom, Thiruvananthapuram – 695581, Kerala ,INM. C. Subhash Peter
DOI:
https://doi.org/10.18311/jer/2018/24149Keywords:
Anabas testudineus, Cytochrome oxidase, Fish Stress, Hypoxia ROS, Mitochondria Energetics, Nitric OxideAbstract
Nitric oxide (NO), a gaseous free radical that functions as signal molecule, regulates several physiological functions. But in teleost fishes, the influence of NO on mitochondrial energetics is not yet understood. With a view to understanding the short-term in vivo action of NO on mitochondrial energetics in fish, we examined the effects of sodium nitroprusside, a NO donor (SNP) and N-omega-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of nitric oxide synthase (L-NAME), on major electron carriers and oxidative status in heart and liver mitochondria of an obligate air-breathing fish (Anabas testudineus Bloch) kept at either non-stressed or hypoxia-stressed condition. The total nitrate/nitrite (NO3-/NO2-) level that corresponds to NO content showed a rise after SNP (5 μg g-1) and a decline in the heart and liver of non-stressed fish after L-NAME (100 ng g-1) treatments for 30 min. Water immersion for 30 min that induced hypoxia lowered NO3-/NO2- level in heart and liver, but showed a rise in NO3-/NO2- level after SNP treatment of immersion-stressed fish. Reactive Oxygen Species (ROS) production increased after SNP treatment but decreased after L-NAME treatment in heart of hypoxia-stressed fish where as in liver both SNP and L-NAME treatments caused decrease of ROS in stressed fish. SNP treatment increased and L-NAME treatment lowered peroxynitrite (ONOO-) level in heart and liver of non-stressed fish. SNP treatment lowered the activity of cytochrome c oxidase (COX) but L-NAME treatment increased its activity in mitochondria of heart of hypoxia-stressed fish. In liver mitochondria, however, COX activity showed a rise after these treatments. On the contrary, SNP and L-NAME treatments in stressed fish elevated succinate dehydrogenase (SDH) activity in both heart and liver mitochondria. In heart, LDH activity increased after SNP and L-NAME treatments in both non-stressed and stressed conditions, but not in liver of stressed fish. Put together, the data provide evidence that NO exerts an integrative action on mitochondrial energetics in heart and liver mitochondria of air-breathing fish during their exposure to hypoxia-stress.
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