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感染白斑综合征病毒(WSSV)的凡纳滨对虾组织防御系统的变化

Changes in tissue defence system in white spot syndrome virus (WSSV) infected Penaeus monodon.

作者信息

Mathew Suseela, Kumar K Ashok, Anandan R, Viswanathan Nair P G, Devadasan K

机构信息

Biochemistry and Nutrition Division, Central Institute of Fisheries Technology, Matsyapuri PO, Cochin 682 029, Kerala, India.

出版信息

Comp Biochem Physiol C Toxicol Pharmacol. 2007 Apr;145(3):315-20. doi: 10.1016/j.cbpc.2007.01.001. Epub 2007 Jan 11.

DOI:10.1016/j.cbpc.2007.01.001
PMID:17287147
Abstract

The present study examined the changes occurring in the pro phenoloxidase system and antioxidant defence status in haemolymph, hepatopancreas and muscle tissue of white spot syndrome virus (WSSV) infected Penaeus monodon. Tiger shrimps (P. monodon) were infected with white spot virus by intramuscular injection of the virus inoculum. Levels of lipid peroxides and the activities of phenoloxidase, glutathione-dependent antioxidant enzymes [glutathione peroxidase (GPX), glutathione-S-transferase (GST)] and antiperoxidative enzymes [superoxide dismutase (SOD) and catalase (CAT)] were determined. WSSV infection induced a significant increase in lipid peroxidation in haemolymph, muscle and hepatopancreas of experimental P. monodon compared to normal controls. This was paralleled by significant reduction in the activities of phenol oxidase, glutathione-dependent antioxidant enzymes and antiperoxidative enzymes. The results of the present study indicate that the tissue antioxidant defence system in WSSV infected P. monodon is operating at a lower rate, which ultimately resulted in the failure of counteraction of free radicals, leading to oxidative stress as evidenced by the increased level of lipid peroxidation.

摘要

本研究检测了感染白斑综合征病毒(WSSV)的凡纳滨对虾血淋巴、肝胰腺和肌肉组织中前酚氧化酶系统的变化以及抗氧化防御状态。通过肌肉注射病毒接种物使凡纳滨对虾(斑节对虾)感染白斑病毒。测定了脂质过氧化物水平以及酚氧化酶、谷胱甘肽依赖性抗氧化酶[谷胱甘肽过氧化物酶(GPX)、谷胱甘肽-S-转移酶(GST)]和抗过氧化酶[超氧化物歧化酶(SOD)和过氧化氢酶(CAT)]的活性。与正常对照组相比,WSSV感染导致实验性凡纳滨对虾血淋巴、肌肉和肝胰腺中的脂质过氧化显著增加。与此同时,酚氧化酶、谷胱甘肽依赖性抗氧化酶和抗过氧化酶的活性显著降低。本研究结果表明,感染WSSV的凡纳滨对虾的组织抗氧化防御系统运行速率较低,最终导致自由基对抗作用失败,脂质过氧化水平升高证明了这会导致氧化应激。

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