GUO Xiaoli, HUANG Zhihui, MA Aijun, WANG Qingmin, XU Rongjing, LI Ming, CHEN Zhixin. Effects of thermal stress on turbot (Scophthalmus maximus) myocardial injury and apoptosis[J]. Journal of fisheries of china, 2022, 46(6): 1074-1084. DOI: 10.11964/jfc.20201112492
Citation: GUO Xiaoli, HUANG Zhihui, MA Aijun, WANG Qingmin, XU Rongjing, LI Ming, CHEN Zhixin. Effects of thermal stress on turbot (Scophthalmus maximus) myocardial injury and apoptosis[J]. Journal of fisheries of china, 2022, 46(6): 1074-1084. DOI: 10.11964/jfc.20201112492

Effects of thermal stress on turbot (Scophthalmus maximus) myocardial injury and apoptosis

  • Scophthalmus maximus is an economic fish adapted to cold water at low temperature and high temperature severely affects its growth and survival. Scolars have confirmed that heart function is an important factor in setting the upper limit of heat range for fish. The present study aimed to investigate the damage of thermal stress on turbot heart and its mechanism in terms of physiologic, biochemical response and apoptosis gene expression levels. In this study, we investigated the characterization and mechanism response to thermal stress in the heart, using H.E staining, electron microscopic observation, enzyme activity detection and qPCR. The results showed that the aggravated degrees of swelling and breakage of myocardial fiber, dilatation of interstitial space, inflammatory cell infiltration, mitochondrial structure destruction and other tissue damage with the elevated temperature, but the tissue damage was significantly reduced at 24 °C-24 h. CK activity increased significantly with the escalation of thermal stress; LDH, SOD activity and MDA content reached their peak at 24 °C. Expression levels of Bax and Caspase-3 decreased significantly after thermal tress, while, the expression level of Bcl-2 gradually increased. These results indicated that the myocardium could reduce the expression of Bax and Caspase-3 genes and promote the expression of the anti-apoptotic gene Bcl-2 to reduce the loss of myocardial cells to reduce thermal stress damage when it suffered a lesser degree of heat stress. This suggested that thermal stress causes the heart defense enzymes to exert resistance to maintains body homeostasis. The organism defense system itself is damaged because the heat stress exceeds its own physiological regulation threshold when the heat stress intensifies to 28 °C, causing severely damages of heart structure and even leads to death in turbot. The results showed that thermal stress causes myocardial damage of turbot, and the body maintains homeostasis via regulating the activity of defense enzymes and apoptosis pathway related genes. This study provides a theoretical basis for subsequent research of the physiological adaptation mechanism of turbot's and other fishes' heart against thermal stress. At the same time, it provides more trait indicators for the high temperature tolerance traits to improve the breeding accuracy of marine fish.
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