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盐度胁迫对大黄鱼能量代谢与线粒体自噬的影响OA北大核心CSTPCD

SALINITY STRESS ON ENERGY METABOLISM AND MITOCHONDRIAL AUTOPHAGY IN LARGE YELLOW CROAKER

中文摘要英文摘要

为了比较高盐和低盐胁迫对大黄鱼(Larimichthys crocea)肝脏能量代谢和线粒体自噬的影响差异及其作用机制,将体质量为(53.46±1.47)g大黄鱼放入盐度为12、25或40的水体暴露1d、3d和7d,取其肝脏样本检测氧化损伤、能量代谢和线粒体自噬相关指标.结果显示,胁迫1d时,高盐组的大黄鱼肝脏三羧酸循环酶活力和线粒体自噬基因表达水平显著高于低盐组,表明鱼类在盐度胁迫初期需要消耗更多的能量,并提高线粒体自噬来应对高盐胁迫.胁迫7d时,高盐组的大黄鱼肝脏ATP合成酶活力和微管相关蛋白轻链3基因表达水平低于低盐组,活性氧簇和乳酸含量,乙酰辅酶A羧化酶活力高于低盐组,表明高盐组的大黄鱼在胁迫末期降低了有氧代谢和线粒体自噬,提高了无氧代谢,导致机体能量供应不足,线粒体自噬受到抑制,从而加重了鱼类氧化损伤.在盐度胁迫过程中,腺苷酸活化蛋白激酶和叉头框转录因子O亚型3分别在调控能量代谢酶活力和线粒体自噬基因表达方面发挥重要作用.研究结果揭示了高盐和低盐胁迫对大黄鱼能量代谢与线粒体自噬的影响差异及其初步机制,可为大黄鱼养殖水体的盐度调节方案制定及养殖水域选择提供基础资料.

Large yellow croaker(Larimichthys crocea)is an important marine economic fish in China,however,it faces challenges such as insufficient aquaculture water,severe water pollution,and frequent occurrence of diseases.Expand-ing cultivation from the inner bay to the outer sea can address these issues,but varying water salinity across sea areas poses a hurdle.Thus,it is necessary to understand the impact of salinity changes on fish physiology.This study aimed to compare how high and low salinity affect energy metabolism and mitophagy in the liver of large yellow croaker and elucidate the underlying mechanism.Fish weighing(53.46±1.47)g were obtained from Fufa Aquatic Co.Ltd.(Ningde,China)and randomly placed in 400 L fiberglass tanks(9 tanks)with seawater salinity at 12,25 or 40.This setup was maintained for 1d,3d and 7d,with three replicates for each salinity group.Measurements included oxidative damage markers(radical oxygen species(ROS)),energy metabolism indicators(adenosine triphosphate(ATP)and lactate contents;pyruvate kinase(PK),lactic dehydrogenase(LDH),succinate dehydrogenase(SDH),malate dehydrogenase(MDH),ATP synthase(F-ATP),carnitine palmitoyl transterase-1(CPT-1),acetyl-CoA carboxylase(ACC)and adeno-sine 5'-monophosphate(AMP)-activated protein kinase(AMPK)enzyme activities),and mitochondrial autophagy indi-cators(microtubule-associated protein light chain 3(LC3α),PTEN induced putative kinase 1(PINK1),Parkin,mito-fusin 2(Mfn2)and forkhead box class O3(FoxO3)gene expression levels).The results showed that tricarboxylate cyclase enzyme(SDH,MDH and F-ATP)activities and mitophagy gene(LC3α,PINK1,Parkin,Mfn2)expression levels in the high-salt group were significantly higher than those in the low-salt group on day 1,indicating that increased energy consumption and enhanced mitophagy to cope with early high-salt stress.The high-salt group increased fatty acid β oxidase enzyme(CPT-1)activities,and reduced F-ATP activity and LC3 α gene expression levels on day 3,resulting in increased lactate and ROS contents.F-ATP activity and LC3α gene expression levels in the high-salt group were lower while ROS and lactate contents and acetyl ACC activity were higher than those in the low-salt group on day 7,suggesting a shift toward decreased aerobic metabolism,reduced mitophagy,and increased anaerobic metabolism,leading to insufficient energy supply,loss of mitophagy function,and exacerbated oxidative damage.Furthermore,gene expressions of AMPK and FoxO3 positively correlated with mRNA levels of energy metabolism and mitophagy related genes,respectively,indicating that AMPK and FoxO3 played important roles in regulating energy metabolism enzyme activities and mitophagy gene expressions during the salinity stress.In conclusion,research results highlight the differences in the effects of high and low salinity on energy metabolism and mitophagy in large yellow croaker.These findings provide basic data for formulating salinity regulation plans and selecting suitable aquaculture water bodies for large yellow croaker.

曾霖;熊逸飞;宋炜;谢正丽;王永红

蚌埠学院食品与生物工程学院,蚌埠 233030中国水产科学研究院东海水产研究所,上海 200090||上海海洋大学水产与生命学院,上海 201306中国水产科学研究院渔业机械仪器研究所,上海 200090

生物学

能量代谢线粒体自噬盐度胁迫大黄鱼

Energy metabolismMitophagySalinity stressLarimichthys crocea

《水生生物学报》 2024 (005)

725-733 / 9

青岛海洋科技中心山东省专项经费(2022QNLM30001);国家重点研发计划(2022YFD2401102);中国水产科学研究院基本科研业务费(2020TD76)资助[Supported by the Marine S & T Fund of Shandong Province for Pilot National Laboratory for Marine Science and Technology(Qingdao)(2022QNLM30001);National Key Research and Development Program of China(2022YFD 2401102);Central Public-interest Scientific Institution Basal Research Fund,CAFS(2020TD76)]

10.7541/2024.2023.0341

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