Se(Ⅳ)和Se(Ⅵ)在斑马鱼组织中的累积及对抗氧化系统的影响
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摘要
以斑马鱼为受试材料,研究了Se(Ⅳ)和Se(Ⅵ)在斑马鱼组织中的累积及对抗氧化系统的影响。试验分3组,分别为对照组、Se(Ⅳ)处理组(500μg·L-1)和Se(Ⅵ)处理组(5000μg·L-1),处理28 d后,测定斑马鱼脑、鳃、肝、肠和肌肉组织中硒的累积以及过氧化氢酶(CAT)活性、总抗氧化能力(T-AOC)和Na+/K+-ATPase活性。结果显示,与对照组相比,硒处理组斑马鱼各组织中呈现不同程度的硒累积,肝组织中硒累积量最高,肠组织中CAT活性、鳃和肠组织中T-AOC活性以及鳃和肝组织中Na+/K+-ATPase活性均显著降低。Se(Ⅳ)与Se(Ⅵ)处理组相比,斑马鱼肝和鳃组织中硒累积量显著升高,肝组织中CAT活性显著下降13%,T-AOC活性显著升高1.8倍。研究结果表明Se(Ⅳ)比Se(Ⅵ)生物可利用性更高,硒累积导致斑马鱼组织发生氧化胁迫,试验为进一步从抗氧化系统的角度研究硒暴露对鱼类等水生生物的毒性作用机制奠定了基础。
This study aimed to explore the effects of Se(Ⅳ)and Se(Ⅵ)exposure on the antioxidant system and Se accumulation in ze-brafish(Danio rerio)tissues. The study organisms were divided into three groups, i.e., control group, Se(Ⅳ)-exposed group(500 μg·L-1),and Se(Ⅵ)-exposed group(5000 μg·L-1). The Se accumulation, catalase(CAT), total antioxidant capacity(T-AOC), and Na+/K+-ATPaseactivity were determined in the brain, gill, liver, intestine, and muscle tissues of zebrafish after exposure to both Se species for 28 days. Theresults showed different extents of Se accumulation in fish tissues from the Se-exposed groups compared with the control treatment. The ac-cumulation of Se in the liver was the highest. CAT activity in the intestine, T-AOC activity in the gills and intestine, and Na+/K+-ATPase ac-tivity in the gills and liver tissues were significantly decreased. As compared with the Se(Ⅵ)treatment, Se accumulation in the liver andgill tissues of fish was significantly elevated in the Se(Ⅳ)treatment. CAT activity in the liver was significantly decreased 13%. However,the T-AOC was significantly increased 1.8 times. These results demonstrated that Se(Ⅳ)is more bioavailable than Se(Ⅵ). Se accumula-tion caused oxidative stress in zebrafish tissues. Our findings represent a progress in research on the toxicological mechanism of Se exposurein fish and other aquatic organisms from the aspects of the antioxidant defense system.
This study aimed to explore the effects of Se(Ⅳ)and Se(Ⅵ)exposure on the antioxidant system and Se accumulation in ze-brafish(Danio rerio)tissues. The study organisms were divided into three groups, i.e., control group, Se(Ⅳ)-exposed group(500 μg·L-1),and Se(Ⅵ)-exposed group(5000 μg·L-1). The Se accumulation, catalase(CAT), total antioxidant capacity(T-AOC), and Na+/K+-ATPaseactivity were determined in the brain, gill, liver, intestine, and muscle tissues of zebrafish after exposure to both Se species for 28 days. Theresults showed different extents of Se accumulation in fish tissues from the Se-exposed groups compared with the control treatment. The ac-cumulation of Se in the liver was the highest. CAT activity in the intestine, T-AOC activity in the gills and intestine, and Na+/K+-ATPase ac-tivity in the gills and liver tissues were significantly decreased. As compared with the Se(Ⅵ)treatment, Se accumulation in the liver andgill tissues of fish was significantly elevated in the Se(Ⅳ)treatment. CAT activity in the liver was significantly decreased 13%. However,the T-AOC was significantly increased 1.8 times. These results demonstrated that Se(Ⅳ)is more bioavailable than Se(Ⅵ). Se accumula-tion caused oxidative stress in zebrafish tissues. Our findings represent a progress in research on the toxicological mechanism of Se exposurein fish and other aquatic organisms from the aspects of the antioxidant defense system.
引文
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[10] Valko M, Morris H, Cronin M T. Metals, toxicity and oxidative stress[J]. Current Medicinal Chemistry, 2005, 12(10):1161-1208.
[11] Lemly A D. A teratogenic deformity index for evaluating impacts of selenium on fish populations[J]. Ecotoxicology and Environmental Safety, 1997, 37(3):259-266.
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[14] Hoffman D J. Role of selenium toxicity and oxidative stress in aquatic birds[J]. Aquatic Toxicology, 2002, 57(1/2):11-26.
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[19]李保民.环境中的硒-生物效应、形态、浓度水平及人体摄入标准[J].环境保护科学, 1988, 14(1):66-72.LI Bao-min. Selenium in the environment:Biological effect, forms,concentration level and human consumption standard[J]. Environmental Protection Science, 1988, 14(1):66-72.
[20] Maier K J, Knight A W. Ecotoxicology of selenium in freshwater systems[J]. Reviews of Environmental Contamination and Toxicology,1994, 134:31-48.
[21] Miller L L, Wang F, Palace V P, et al. Effects of acute and subchronic exposures to waterborne selenite on the physiological stress response and oxidative stress indicators in juvenile rainbow trout[J]. Aquatic Toxicology, 2007, 83(4):263-271.
[22] Orun I, Talas Z S, Ozdemir I, et al. Antioxidative role of selenium on some tissues of(Cd2+, Cr3+)-induced rainbow trout[J]. Ecotoxicology and Environmental Safety, 2008, 71(1):71-75.
[23] Misra S, Niyogi S. Selenite causes cytotoxicity in rainbow trout(Oncorhynchus mykiss)hepatocytes by inducing oxidative stress[J]. Toxicology in Vitro, 2009, 23(7):1249-1258.
[24] Abbas H H H, Authman M M N. Effects of accumulated selenium on some physiological parameters and oxidative stress indicators in Tilapia fish(Oreochromis spp.)[J]. American-Eurasian Journal of Agricultural and Environmental Science, 2009, 5(2):219-225.
[25] Xie L T, Wu X, Chen H X, et al. The bioaccumulation and effects of selenium in the oligochaete Lumbriculus variegatus via dissolved and dietary exposure routes[J]. Aquatic Toxicology, 2016, 178:1-7.
[26] Jagoe C H, Shaw-Allen P L, Brundage S. Gill Na+, K+-ATPase activity in largemouth bass(Micropterus salmoides)from three reservoirs with different levels of mercury contamination[J]. Aquatic Toxicology, 1996,36(3):161-176.
[27] Morgan I J, Henry R P, Wood C M. The mechanism of acute silver nitrate toxicity in freshwater rainbow trout(Oncorhynchus mykiss)is inhibition of gill Na+and Cl-transport[J]. Aquatic Toxicology, 1997, 38(96):145-163.
[28]贾秀英,陈志伟.铜、镉对鲫鱼组织Na+-K+-ATPase酶活性的影响[J].科技通报, 2003, 19(1):50-53.JIA Xiu-ying, CHEN Zhi-wei. Effects of copper and cadmium on Na+-K+-ATPase activity in tissues of Carassius auratus[J]. Bulletin of Science and Technology, 2003, 19(1):50-53.
[29]袁锦芳,陈叙龙,张毓琪.环境因素对海洋动物Na+-K+-ATPase的影响概述[J].海洋环境科学, 1999, 18(3):75-79.YUAN Jin-fang, CHEN Xu-long, ZHANG Yu-qi. Effects of the environmental factors on Na+-K+-ATPase of marine animals[J]. Marine Environmental Science, 1999, 18(3):75-79.
[30] Ates B, Orun I, Talas Z S, et al. Effects of sodium selenite on some biochemical and hematological parameters of rainbow trout(Oncorhynchus mykiss Walbaum, 1792)exposed to Pb2+and Cu2+[J]. Fish Physiology and Biochemistry, 2008, 34(1):53-59.
[31] Ralston N V, Raymond L J. Dietary selenium′s protective effects against methylmercury toxicity[J]. Toxicology, 2010, 278(1):112-123.
[32] Bjerregaard P, Fjordside S, Hansen M G, et al. Dietary selenium reduces retention of methylmercury in freshwater fish[J]. Environmental Science and Technology, 2011, 45(22):9793-9798.
[33] U.S. Geological Survey. Bioaccumulation and toxicity of selenium during a life-cycle exposure with desert pupfish(Cyprinodon macularius)[R]. Columbia:U. S. Geological Survey Scientific Investigations Report, 2012.
[34] Manduzio H, Monsinjon T, Rocher B, et al. Characterization of an inducible isoform of the Cu/Zn superoxide dismutase in the blue mussel Mytilus edulis[J]. Aquatic Toxicology, 2003, 64(1):73-83.
[35]王春凤.硒对汞致剑尾鱼抗氧化系统的毒害和生理损伤的拮抗作用[D].广州:华南师范大学, 2004.WANG Chun-feng. The antagonistic action of selenium on the harm of antioxidant system and physiological damage in swordtail fish(Xiphophorus helleri)under the exposure of mercury[D]. Guangzhou:South China Normal University, 2004.
[36] Ma S S, Zhou Y, Chen H X, et al. Selenium accumulation and the effects on the liver of topmouth gudgeon Pseudorasbora parva exposed to dissolved inorganic selenium[J]. Ecotoxicology and Environmental Safety, 2018, 160:240-248. Doi:10.1016/j.ecoenv.2018.05.047.
[37] Oberemm A. The use of a refined zebrafish embryo bioassay for the assessment of aquatic toxicity[J]. Laboratory Animals, 2000, 29(7):32-40.
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