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瓦氏黄颡鱼肠道在长期低氧胁迫下的氧化应激、细胞凋亡和免疫反应。

Long-term hypoxia stress-induced oxidative stress, cell apoptosis, and immune response in the intestine of Pelteobagrus vachelli.

机构信息

College of Marine Science and Engineering, Jiangsu Province Engineering Research Center for Aquatic Animals Breeding and Green Efficient Aquacultural Technology, Nanjing Normal University, Nanjing, 210023, China.

Co-Innovation Center for Marine Bio-Industry Technology of Jiangsu Province, Lianyungang, 222005, Jiangsu, China.

出版信息

Fish Physiol Biochem. 2023 Aug;49(4):585-597. doi: 10.1007/s10695-023-01204-6. Epub 2023 May 24.

DOI:10.1007/s10695-023-01204-6
PMID:37222964
Abstract

Hypoxia is a common phenomenon in aquaculture. With the dissolved oxygen (DO) 3.75 ± 0.25 mg O /L for hypoxia group and 7.25 ± 0.25 mg O /L for control group for 30, 60, and 90 days, long-term hypoxia stress was used to investigate the oxidative stress, apoptosis, and immunity in the intestine of Pelteobagrus vachelli. According to the results of measurement of total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-PX), and catalase (CAT) activities and malondialdehyde (MDA) content, the oxidative stress ability of the intestine was activated at 30 days and impaired at 60 and 90 days. The upregulation of Bcl-2-associated x (Bax); downregulation of B cell lymphoma-2 (Bcl-2); increased activities of caspase-3, caspase-9, and Na-K-ATPase; decreased activities of succinate dehydrogenase (SDH); and the release of cytochrome c (Cyt-c) in mitochondria revealed that hypoxia induced the apoptosis. Moreover, heat shock protein 70 (HSP 70), heat shock protein 90 (HSP 90), immunoglobulin M (IgM), and C-lysozyme (C-LZM) were activated to inhibit apoptosis, but the immunoregulatory function might be damaged at 60 and 90 days. This study provides a theoretical foundation for understanding the mechanisms of hypoxia stress and aquaculture management of P. vachelli.

摘要

缺氧是水产养殖中常见的现象。采用溶解氧(DO)为 3.75±0.25mg O/L 的低氧组和 7.25±0.25mg O/L 的对照组,分别处理 30、60 和 90 天,研究了长期低氧胁迫对瓦氏黄颡鱼肠道氧化应激、凋亡和免疫的影响。根据总超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-PX)和过氧化氢酶(CAT)活性以及丙二醛(MDA)含量的测定结果,肠道的氧化应激能力在 30 天时被激活,而在 60 和 90 天时受到损害。Bcl-2 相关 X(Bax)上调;B 细胞淋巴瘤-2(Bcl-2)下调;半胱天冬酶-3、半胱天冬酶-9 和 Na-K-ATP 酶活性增加;琥珀酸脱氢酶(SDH)活性降低;以及线粒体中细胞色素 c(Cyt-c)的释放表明,缺氧诱导了细胞凋亡。此外,热休克蛋白 70(HSP 70)、热休克蛋白 90(HSP 90)、免疫球蛋白 M(IgM)和 C-溶菌酶(C-LZM)被激活以抑制凋亡,但在 60 和 90 天时,免疫调节功能可能受损。本研究为了解黄颡鱼缺氧应激机制和水产养殖管理提供了理论基础。

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