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细鳞鲑(鲑科)对严重热应激的氧化还原状态和代谢反应。

Redox state and metabolic responses to severe heat stress in lenok (Salmonidae).

作者信息

Chen Yan, Pan Zhe, Bai Yucen, Xu Shaogang

机构信息

National Engineering Research Center for Freshwaters (Beijing), Fisheries Science Institute, Beijing Academy of Agriculture and Forestry Sciences, Beijing, China.

Ocean College of Hebei Agricultural University, Qinhuangdao, Hebei Province, China.

出版信息

Front Mol Biosci. 2023 May 24;10:1156310. doi: 10.3389/fmolb.2023.1156310. eCollection 2023.

DOI:10.3389/fmolb.2023.1156310
PMID:37293553
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10244579/
Abstract

In order to provide new insights into the physiological responses of lenok (: Salmonidae) to acute and severe heat stress (25°C, 48 h), dynamic changes in redox state and metabolic responses are studied combined biochemical index and non-targeted metabolome. Nicotinamide adenine dinucleotide (NAD) consumption causes significant increases in ratio of reduced NADH to NAD and ratio of reduced nicotinamide adenine dinucleotide phosphate (NADPH) to NADP, which induced the redox imbalance in heat stressed lenok. Lowered reduced glutathione/oxidized glutathione (GSH/GSSG) ratios suggested that more oxidized conditions occurred in heat-stressed lenok, leading to membrane lipid oxidation. The first few hours of heat stress promoted the activity of enzymes involved in anaerobic glycolysis (hexokinase, pyruvate kinase, lactic dehydrogenase) and glutamicpyruvic transaminase and glutamic oxaloacetic transaminase, which might lead to consumption of many carbohydrates and amino acid catabolism. These enzyme activities decreased with time in a possible compensatory strategy to manage anabolic and catabolic metabolism, maintaining the redox homeostasis. After 48 h of recovery, NAD, carbohydrate levels and enzyme activities had returned to control levels, whereas many amino acids were consumed for repair and new synthesis. GSH remained at levels lower than controls, and the more oxidized conditions had not recovered, aggravating oxidative damage. Glutamic acid, glutamine, lysine and arginine may play important roles in survival of heat-stressed lenok.

摘要

为了深入了解细鳞鲑(鲑科)对急性严重热应激(25°C,48小时)的生理反应,结合生化指标和非靶向代谢组学研究了氧化还原状态的动态变化和代谢反应。烟酰胺腺嘌呤二核苷酸(NAD)的消耗导致还原型NADH与NAD的比率以及还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)与NADP的比率显著增加,这在热应激的细鳞鲑中诱导了氧化还原失衡。还原型谷胱甘肽/氧化型谷胱甘肽(GSH/GSSG)比率降低表明热应激的细鳞鲑中出现了更多的氧化状态,导致膜脂氧化。热应激的最初几个小时促进了参与无氧糖酵解的酶(己糖激酶、丙酮酸激酶、乳酸脱氢酶)以及谷丙转氨酶和谷草转氨酶的活性,这可能导致许多碳水化合物的消耗和氨基酸分解代谢。随着时间的推移,这些酶的活性下降,这可能是一种管理合成代谢和分解代谢的补偿策略,以维持氧化还原稳态。恢复48小时后,NAD、碳水化合物水平和酶活性已恢复到对照水平,而许多氨基酸被用于修复和新合成。谷胱甘肽水平仍低于对照,且氧化程度更高的状态尚未恢复,加剧了氧化损伤。谷氨酸、谷氨酰胺、赖氨酸和精氨酸可能在热应激细鳞鲑的存活中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/4b3ed1e785fe/fmolb-10-1156310-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/d2ed1eb521ea/fmolb-10-1156310-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/ba5f1997cc4a/fmolb-10-1156310-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/42999b9922bd/fmolb-10-1156310-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/4b3ed1e785fe/fmolb-10-1156310-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/d2ed1eb521ea/fmolb-10-1156310-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/37017d2dc1cc/fmolb-10-1156310-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/7e47431e6c38/fmolb-10-1156310-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/ba5f1997cc4a/fmolb-10-1156310-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/42999b9922bd/fmolb-10-1156310-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf74/10244579/4b3ed1e785fe/fmolb-10-1156310-g006.jpg

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