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Oxidative Stress Responses and Recovery Patterns in the Liver of Oreochromis niloticus Exposed to Chlorpyrifos-Ethyl

机译:毒死rif-乙基暴露对尼罗罗非鱼肝脏的氧化应激反应和恢复模式

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摘要

Chlorpyrifos is the most common insecticide in freshwater ecosystems, and detected in agricultural and fishery product. In this study, Oreochromis niloticus were exposed to 5, 10 and 15 ppb sublethal concentrations of chlorpyrifos in order to determine the oxidative stress response in liver. Acetylcholinesterase (AChE) activity was significantly inhibited. Superoxide dismutase activity (SOD) increased after 15 days of chlorpyrifos treatments at all concentrations (146.95%, 53.04%, 208.70%, respectively). Malondialdehyde levels were higher than that of the control level after 15 days of 5 ppb (95.65%), 10 ppb (69.56%) and 15 ppb (252.17%) chlorpyrifos treatments. Malondialdehyde levels were also increased ranging from 59.09%, 113.63% to 195.46% after 30 days of 5, 10 and 15 ppb chlorpyrifos exposures. Glutathione S-transferase activity decreased except for 15 days low concentration exposure. Catalase (CAT) activity decreased while there is no significant alteration in glutathione peroxidase activity. After recovery period, the low concentration group of chlorpyrifos provided a protection in AChE activity during recovery, but fish were observed to be unable to overcome the inhibition of AChE activity at high concentration groups. CAT activity remained reduced, SOD activity increased whereas the other biochemical parameters recovered to control levels. Results of this study suggest that chlorpyrifos induces oxidative stress in the liver of O. niloticus and this effect is not related with anti-acetylcholinesterase activity of pesticide.
机译:毒死rif是淡水生态系统中最常见的杀虫剂,并在农业和渔业产品中检出。在这项研究中,尼罗罗非鱼(Oreochromis niloticus)暴露于5、10和15 ppb亚致死浓度的毒死rif以确定肝脏中的氧化应激反应。乙酰胆碱酯酶(AChE)活性被显着抑制。在所有浓度下毒死rif处理15天后,超氧化物歧化酶活性(SOD)均升高(分别为146.95%,53.04%,208.70%)。在5 ppb(95.65%),10 ppb(69.56%)和15 ppb(252.17%)毒死rif处理15天后,丙二醛水平高于对照水平。在5、10和15 ppb毒死rif暴露30天后,丙二醛水平也从59.09%,113.63%增至195.46%。谷胱甘肽S-转移酶活性降低,除了低浓度暴露15天。过氧化氢酶(CAT)活性降低,而谷胱甘肽过氧化物酶活性没有明显改变。恢复期过后,低浓度毒死group在恢复过程中对AChE活性提供了保护,但观察到鱼无法克服高浓度组对AChE活性的抑制作用。 CAT活性仍然降低,SOD活性增加,而其他生化参数恢复到控制水平。这项研究的结果表明毒死rif可以诱导尼罗罗非鱼肝脏中的氧化应激,而这种作用与农药的抗乙酰胆碱酯酶活性无关。

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