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首页> 外文期刊>Journal of biochemical and molecular toxicology >Piperonyl butoxide increases oxidative toxicity of fenthion in the brain of oreochromis niloticus
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Piperonyl butoxide increases oxidative toxicity of fenthion in the brain of oreochromis niloticus

机译：胡椒基丁醚增加尼罗罗非鱼脑中倍硫磷的氧化毒性

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摘要

The present study was designed to understand the effects of piperonyl butoxide (PBO), modulator of cytochrome P450 (CYP 450), on the neurotoxicity of organophosphate pesticide fenthion in the brain of Oreochromis niloticus used as a model organism. Fish were exposed to one-fourth of the LC50 value of fenthion (0.567 mg/L) and 0.5 mg/L PBO concentration for 24 h, 96 h, and 15 days. Glutathione (GSH)-related antioxidant system, lipid peroxidation, stress proteins, and acetylcholinesterase (AchE) activity were investigated. Our results showed that PBO induced the neurotoxic effect of fenthion with increasing oxidative stress in long-term exposure. GSH-related antioxidant system might take a role in protecting the brain from these oxidative effects. PBO possibly inhibited the biotransformation of fenthion by inhibiting CYP 450; thereby preventing the brain from AChE inhibition in short-term exposure. Changes in parameters indicated that PBO caused biphasic response by affecting CYP 450 in the brain of O. niloticus.
机译：本研究旨在了解细胞色素P450（CYP 450）的调节剂胡椒基丁醚（PBO）对用作模型生物的尼罗罗非鱼脑中有机磷酸酯杀虫剂硫磷的神经毒性。将鱼暴露在二氧化硫的LC50值的四分之一（0.567 mg / L）和0.5 mg / L PBO浓度下持续24 h，96 h和15天。谷胱甘肽（GSH）相关的抗氧化剂系统，脂质过氧化，应激蛋白和乙酰胆碱酯酶（AchE）活性进行了调查。我们的结果表明，PBO在长期暴露中随着氧化应激的增加而诱导了对硫磷的神经毒性作用。与GSH相关的抗氧化剂系统可能在保护大脑免受这些氧化作用方面起作用。 PBO可能通过抑制CYP 450而抑制了硫磷的生物转化。从而防止大脑在短期暴露中抑制AChE。参数的变化表明，PBO通过影响尼罗罗非鱼大脑中的CYP 450引起两相反应。

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