文献类型: 外文期刊
作者: Jia, Yudong 1 ; Wang, Feng 1 ; Chen, Shuaiyu 1 ; Wang, Jiawei 1 ; Gao, Yuntao 1 ;
作者机构: 1.Chinese Acad Fishery Sci, Qingdao Key Lab Marine Fish Breeding & Biotechnol, Yellow Sea Fisheries Res Inst, 106 Nanjing Rd, Qingdao 266071, Peoples R China
2.Shanghai Ocean Univ, Coll Fisheries & Life Sci, Shanghai, Peoples R China
关键词: Hypoxia stress; Metabolism; Oxidative stress; Gill histology; Turbot Scophthalmus maximus. L
期刊名称:FISH PHYSIOLOGY AND BIOCHEMISTRY ( 影响因子:2.5; 五年影响因子:2.7 )
ISSN: 0920-1742
年卷期: 2024 年
页码:
收录情况: SCI
摘要: Hypoxia affects fish's survival, growth, and physiological metabolism processes. In this study, turbot plasma glucose and cortisol contents, hepatic glycolysis (hexokinase [HK], phosphofructokinase [PFK], pyruvate kinase [PK]) and lipolysis (fatty acid synthetase [FAS], lipoprotein lipase [LPL]) enzyme activities, anti-oxidant enzyme (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GSH-Px]) activities, malondialdehyde (MDA), lactate and glycogen contents, gill histological parameters (lamellar length [SLL], width [SLW], interlamellar distance [ID]), respiratory frequency (RF), the proportion of the secondary lamellae available for gas exchange (PAGE), and hifs (hif-1 alpha, hif-2 alpha, hif-3 alpha) expression were determined during long-term hypoxia and reoxygenation. Results showed that long-term hypoxia (3.34 +/- 0.17 mg L-1) significantly elevated plasma cortisol and glucose contents; increased hepatic HK, PK, PFK, FAS, and LPL activity; decreased hepatic glycogen, lactate contents, and lipid drop numbers; and caused changes of hepatocyte (vacuolation, pyknotic, and lytic nucleus) after treatment for 4 weeks. Hepatic SOD, CAT, GSH-Px activity, and MDA contents; lamellar perimeter, SLL, ID, RF, and PAGE; and hepatic hif-1 alpha, hif-2 alpha, and hif-3 alpha manifested similar results. Meanwhile, hif-1 alpha is significantly higher than hif-2 alpha, and hif-3 alpha. Interestingly, females and males demonstrated no sex dimorphism significantly different from the above parameters (except hepatic FAS, LPL activity, and lipid drop number) under hypoxia. The above parameters recovered to normal levels after reoxygenation treatment for 4 weeks. Thus, long-term hypoxia promotes turbot hepatic glycogenolysis and lipolysis, induces oxidative damage and stimulates hepatic antioxidant capacity, and alters gill morphology to satisfy insufficient energy demand and alleviate potential damage, while hif-1 alpha plays critical roles in the above physiological process.
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