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慢性氨氮暴露诱发黄颡鱼幼鱼谷氨酰胺积累、氧化损伤及免疫抑制的研究
引用本文:黎庆,龚诗雁,黎明.慢性氨氮暴露诱发黄颡鱼幼鱼谷氨酰胺积累、氧化损伤及免疫抑制的研究[J].水产学报,2015,39(5):728-734.
作者姓名:黎庆  龚诗雁  黎明
作者单位:宁波大学海洋学院,浙江宁波,315211
基金项目:浙江省自然科学基金(LQ14C190003);宁波大学科研基金(XYL14006);宁波大学人才工程专项(ZX2013000786)
摘    要:为了研究慢性氨氮胁迫对黄颡鱼幼鱼生长性能、大脑谷氨酰胺积累、肝脏抗氧化酶活性、非特异性免疫应答及抗嗜水气单胞菌感染能力的影响,实验挑选初始体质量为(1.94±0.05)g的健康黄颡鱼幼鱼180尾,开展为期56 d的慢性氨氮胁迫实验.结果表明,实验鱼的终末体质量、增重及饲料效率,氨氮组与对照组无显著性差异,但肝体比氨氮组显著高于对照组;氨氮组实验鱼大脑中氨氮和谷氨酰胺含量显著高于对照组,但谷氨酸含量各组间无显著性差异;氨氮组实验鱼肝脏中超氧化物歧化酶、过氧化物酶及谷胱甘肽过氧化物酶活性显著低于对照组,但硫代巴比妥酸反应物含量氨氮组显著高于对照组;氨氮组实验鱼肝脏中溶菌酶活性、头肾巨噬细胞吞噬指数和呼吸爆发显著低于对照组;感染嗜水气单胞菌14d后,氨氮组和对照组实验鱼累计死亡率无显著性差异.研究表明,黄颡鱼幼鱼遭受亚致死浓度的慢性氨氮胁迫,能够导致大脑中谷氨酰胺含量升高;氨氮组黄颡鱼肝脏中硫代巴比妥酸反应物的过度积累表明,应激产生的大量自由基并不能被机体自身的抗氧化酶体系完全清除;亚致死浓度的慢性氨氮胁迫会对黄颡鱼幼鱼的免疫应答体系造成抑制.

关 键 词:黄颡鱼  氨氮  生长性能  氧化损伤  免疫抑制
收稿时间:2014/12/24 0:00:00
修稿时间:2/9/2015 12:00:00 AM

Chronic ammonia toxicity induces glutamine accumulation, oxidative damage and immunosuppression of juvenile yellow catfish Pelteobagrus fulvidraco
LI Qing,GONG Shiyan and LI Ming.Chronic ammonia toxicity induces glutamine accumulation, oxidative damage and immunosuppression of juvenile yellow catfish Pelteobagrus fulvidraco[J].Journal of Fisheries of China,2015,39(5):728-734.
Authors:LI Qing  GONG Shiyan and LI Ming
Institution:School of Marine Sciences, Ningbo University, Ningbo 315211, China,School of Marine Sciences, Ningbo University, Ningbo 315211, China and School of Marine Sciences, Ningbo University, Ningbo 315211, China
Abstract:A study was carried out to test the responses of juvenile yellow catfish Pelteobagrus fulvidraco to ammonia stress and bacterial challenge. The catfish(1. 94 ± 0. 05)g were randomly allocated to 2 groups(control group and exposure group)in triplicate for 56 days ammonia exposure. No differences were found in fish final weight, weight gain and feed efficiency between ammonia group and control group, but hepatosomatic index of fish in ammonia group was significantly higher than that of fish in control group. Ammonia and glutamine contents in the brain of fish in ammonia group were significantly higher than those of fish in control group, but glutamate content was not significantly different compared with the control. Superoxide dismutase, catalase and glutathione peroxidase activities were significantly lower in ammonia group than in control group, but thiobarbituric acid reactive substance content was significantly higher in ammonia group. Lysozyme activity, phagocytic index and respiratory burst of fish in ammonia group were significantly lower compared with the control group. After 14 days infection of Aeromonas hydrophila, cumulative mortality was not significantly different between ammonia group and control group. This study indicated that the glutamine accumulation in the brain was caused by chronic ammonia exposure; the toxic reactive oxygen species is not fully counteracted by the antioxidant enzymes; the immunosuppression is a process of gradual accumulation of immunosuppressive factors. Our findings support the multifactorial pathogenesis of ammonia toxicity in fish exposed to ammonia.
Keywords:yellow catfish  ammonia  growth performance  oxidative damage  immunosuppression
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