2,4- d和氮磷甲基对尼罗褐虾肝脏抗氧化酶和脂质过氧化的联合影响

Elif Özcan Oruç, Nevin Üner
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引用次数: 171

摘要

本试验旨在研究除草剂2,4- d和杀虫剂氮磷甲基对罗非鱼肝脏抗氧化酶活性和脂质过氧化的影响。将27 ppm 2,4- d、0.03 ppm氮磷甲基和两者的混合物分别暴露24、48、72和96 h。暴露于2,4- d和氮磷甲基的nilochromis肝脏中过氧化氢酶(EC 1.11.1.6)、谷胱甘肽- s转移酶(GST, EC 2.5.1.18)的活性和丙二醛(MDA)的水平,单独和联合暴露均不受农药暴露的影响。单独和联合处理的葡萄糖-6-磷酸脱氢酶(G6PD, EC 1.1.1.49)和谷胱甘肽还原酶(GR, EC 1.6.4.2)活性均显著高于对照组。单独处理时谷胱甘肽过氧化物酶(GPx, EC 1.11.1.9)活性升高,联合处理时该酶活性降低。2,4- d不影响超氧化物歧化酶(SOD, EC 1.15.1.1)活性,但azinphospmethyl处理使SOD活性降低,而联合处理使SOD活性升高。综合处理对SOD活性有增效作用,而对G6PD、GPx、GR活性有拮抗作用。结果表明,niloticus通过抗氧化机制抵抗氧化应激,抑制了脂质过氧化的增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Combined effects of 2,4-D and azinphosmethyl on antioxidant enzymes and lipid peroxidation in liver of Oreochromis niloticus

This study aims to investigate the effects of the herbicide 2,4-D and the insecticide azinphosmethyl on hepatic antioxidant enzyme activities and lipid peroxidation in tilapia. Fish were exposed to 27 ppm 2,4-D, 0.03 ppm azinphosmethyl and to a mixture of both for 24, 48, 72 and 96 h. Activities of catalase (EC 1.11.1.6), glutathione-S-transferase (GST, EC 2.5.1.18) and the level of malondialdehyde (MDA) in the liver of Oreochromis niloticus exposed to 2,4-D and azinphosmethyl, both individually and in combination, were not affected by the pesticide exposures. However, glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49) and glutathione reductase (GR, EC 1.6.4.2) activities in individual and combined treatments, increased significantly compared to controls. Furthermore, glutathione peroxidase (GPx, EC 1.11.1.9) activity increased in individual treatment, while the same enzyme activity decreased in combination. 2,4-D did not affect the activity of superoxide dismutase (SOD, EC 1.15.1.1), but the activity of this enzyme in azinphosmethyl treatment decreased, while its activity increased in combination. Combined treatment of the pesticides exerted synergistic effects in the activity of SOD, while antagonistic effects were found in the activities of G6PD, GPx, GR. The results indicate that O. niloticus resisted oxidative stress by antioxidant mechanisms and prevented increases in lipid peroxidation.

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