Central Inland Fisheries Research Institute (ICAR-CIFRI), Barrackpore, India.
Department of Fishery Sciences, Vidyasagar University, Midnapore, India.
Fish Physiol Biochem. 2021 Feb;47(1):21-32. doi: 10.1007/s10695-020-00880-y. Epub 2020 Oct 14.
Fish mortality generally occurs during extreme summer temperatures in India which are apprehended to be more frequent in near future and may reduce the fish population, particularly in closed aquatic systems. This present study is conducted with the objectives to find out heat shock and associated oxidative stress responses that occurred in selected fish Labeo rohita due to extremely high water temperature (treated, 37-38 °C against control, 28-30 °C) exposure for 2 weeks. Calculated mortality was 30% during the experimental period. The results revealed the biomolecules associated with both the anti-oxidative response (reduced glutathione in serum, liver, muscle; catalase activity in liver, muscle; superoxide dismutase gene expression in the liver) and the heat shock response (hsp70 gene expression in the liver) were elevated under thermal stress. Pro-inflammatory responses (expression of complement protein 3, glyceraldehyde 3-phosphate dehydrogenase in the liver) and oxidative damages (lipid peroxidation in all studied tissue and DNA fragmentation in the liver) were more under thermal stress. Extreme thermal stress induced by partial lethal temperature exposure in this study led to the activation of both the heat shock response and the anti-oxidative response. However, these responses were not elicited to the level so that they can protect from oxidative damages and inflammation in the liver of all the studied fish that caused partial mortality in fish. Thermal stress-induced hepatotoxicity caused fish death which was documented for the first time in freshwater fish.
鱼类死亡率通常发生在印度夏季极端高温期间，预计未来这种情况将更加频繁，可能会减少鱼类数量，尤其是在封闭的水生系统中。本研究旨在探究由于极高水温（处理组 37-38°C，对照组 28-30°C）暴露 2 周而导致的特定鱼类罗非鱼发生的热休克和相关氧化应激反应。在实验期间，死亡率计算为 30%。结果表明，与抗氧化反应相关的生物分子（血清、肝脏、肌肉中的还原型谷胱甘肽；肝脏、肌肉中的过氧化氢酶活性；肝脏中的超氧化物歧化酶基因表达）和热休克反应（肝脏中的 hsp70 基因表达）在热应激下升高。在肝脏中，促炎反应（补体蛋白 3 的表达、甘油醛 3-磷酸脱氢酶）和氧化损伤（所有研究组织中的脂质过氧化和肝脏中的 DNA 片段化）更为严重。本研究中，部分致死温度暴露引起的极端热应激导致了热休克反应和抗氧化反应的激活。然而，这些反应并没有达到足以保护所有研究鱼类肝脏免受氧化损伤和炎症的程度，导致鱼类部分死亡。热应激诱导的肝毒性导致鱼类死亡，这是在淡水鱼类中首次记录到。
