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陈世喜,王鹏飞,区又君,温久福,李加儿,王雯,谢木娇.2016.急性和慢性低氧胁迫对卵形鲳鲹幼鱼肝组织损伤和抗氧化的影响.动物学杂志,51(6):1049-1058.
急性和慢性低氧胁迫对卵形鲳鲹幼鱼肝组织损伤和抗氧化的影响
The Effect of Acute and Chronic Hypoxia Stress on Liver Tissue Structure and Oxidation in Juvenile Golden Pompano (Trachinotus ovatus)
投稿时间:2015-12-28  修订日期:2016-08-22
DOI:DOI: 10.13859/j.cjz.201606013
中文关键词:  卵形鲳鲹  低氧胁迫    氧化应激
英文关键词:Golden Pompano, Trachinotus ovatus  Hypoxia  Liver  Oxidative stress
基金项目:中央级公益性科研院所基本科研业务费专项资金项目(No. 2014TS26),广东省自然科学基金项目(No. 2015A030310253),广东省科技计划项目(No. 2016A0303029);
作者单位E-mail
陈世喜 中国水产科学研究院南海水产研究所上海海洋大学 584112483@qq.com 
王鹏飞 中国水产科学研究院南海水产研究所  
区又君 中国水产科学研究院南海水产研究所 ouyoujun@126.com 
温久福 中国水产科学研究院南海水产研究所  
李加儿 中国水产科学研究院南海水产研究所  
王雯 中国水产科学研究院南海水产研究所上海海洋大学  
谢木娇 中国水产科学研究院南海水产研究所上海海洋大学  
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中文摘要:
      自然海域和养殖水体环境频现低氧,本研究针对卵形鲳鲹(Trachinotus ovatus)不耐低氧的特性,将(31.59 ± 3.01)g(n = 30)的卵形鲳鲹在(23 ± 0.7)℃下进行3、6、12和24 h的急性和14 d的慢性低氧[溶解氧为(1.55 ± 0.20)mg/L]胁迫。运用光学和电子显微技术,比较急、慢性低氧胁迫对卵形鲳鲹肝组织显微和超微结构的影响。通过测定肝组织中的丙二醛(MDA)含量及过氧化氢酶(CAT)、超氧化物歧化酶(SOD)和谷胱甘肽还原酶(GSH)的活性,分析低氧胁迫对卵形鲳鲹肝是否造成氧化损伤。急性低氧胁迫下,卵形鲳鲹肝组织间出现空泡、小叶结构破坏,细胞内线粒体数量减少,出现过氧化物酶体,肝细胞间血窦剧烈扩张。这些病理损伤随胁迫时间延长更趋严重,24 h时甚至出现局部肝细胞融合、坏死,慢性低氧胁迫14 d时,肝细胞局部坏死,细胞膜溶解,细胞核破裂分解,胞质内细胞器不明显,只可分辨粗面内质网,细胞内空泡体积大,细胞结构松散,血窦扩张。急性低氧胁迫下丙二醛(MDA)含量随时间先上升后下降,慢性低氧胁迫14 d时丙二醛(MDA)则显著增加。急性低氧胁迫下超氧化物歧化酶(SOD)和谷胱甘肽还原酶(GSH)上升后恢复,过氧化氢酶(CAT)则持续上调,慢性低氧胁迫下超氧化物歧化酶(SOD)和谷胱甘肽还原酶(GSH)显著上调,过氧化氢酶(CAT)活性下降。结果表明,卵形鲳鲹幼鱼肝组织在低氧胁迫下病理变化明显,氧化损伤严重,且慢性低氧胁迫比急性更甚。
英文摘要:
      Hypoxia occurs in the natural and aquaculture water environment frequently. Golden Pompano (Trachinotus ovatus) is a hypoxia-sensitive fish, so we employed (31.59 ± 3.01g) juvenile golden pompano to study the effect of acute and chronic hypoxia stress on the liver by physiological and histological methods. Individuals were exposed to 3﹣24 h of acute or 14 d of chronic hypoxia stress at room temperature. The histological changes in the liver were observed to analyze the tissue injury. Catalase (CAT), superoxide dismutase (SOD), glutathione (GSH) and malonic dialdehyde (MDA) activities were measured to determine the antioxidant effects in the liver tissue. Data were statistically analyzed. The liver tissue gradually showed vacuoles, expanded blood sinus, and blurred hepatic lobule structure during acute hypoxia. At 24 h acute hypoxia, liver tissue even showed cell fusion and local cell necrosis (Fig. 1e). At 14 d chronic hypoxia, liver tissue showed local cell necrosis and vacuolation inside the cells (Fig. 1f). Cell structure was decentralized, intercellular connection was divided, cell membrane was dissolved, organelles were disrupted, nucleus was decomposed, blood sinus was enlarged, while only rough endoplasmic reticulum was evidently observed (Fig. 2c, d). In acute hypoxia, CAT activity was continuously increased, SOD and GSH activities was recovered after increase (P < 0.05). In chronic hypoxia stress, SOD, GSH activities were significantly increased (P < 0.05), while CAT activity was significantly decreased (P < 0.05) (Fig. 3a﹣c). MDA activity firstly was increased and then recovered in acute hypoxia, but increased significantly (P < 0.05) at 14 d of hypoxia (Fig. 3d). The results show that golden pompano liver tissue structure is seriously damaged and is in severe oxidative stress under hypoxia stress. Hypoxia stress in chronic hypoxia is more serious than that in acute hypoxia.
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