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有机磷农药毒死蜱对神经毒性的诱导作用及牛尿的调节作用。

Induction of neurotoxicity by organophosphate pesticide chlorpyrifos and modulating role of cow urine.

作者信息

Sharma Shelly, Chadha Pooja

机构信息

Cytogenetics Laboratory, Department of Zoology, Guru Nanak Dev University, Amritsar, Punjab 143005 India.

出版信息

Springerplus. 2016 Aug 12;5(1):1344. doi: 10.1186/s40064-016-3004-9. eCollection 2016.

Abstract

INTRODUCTION

Organophosphate pesticides are among the most widely used synthetic chemicals for controlling a wide variety of pests and for domestic purposes. Among these chlorpyrifos (CPF) is the most extensively used pesticide throughout the world, including India.

OBJECTIVE

The present study was undertaken to examine the neurotoxicity induced by CPF and modulatory effect of cow urine as a natural antioxidant alternative to reduce the neurotoxic effects of CPF.

DESIGN

For this purpose LD50 was determined and one fourth of LD50 was selected (38 mg/kg body weight (b.wt)) for treatment of rats. The antioxidant level of cow urine was determined by ABTS assay.

RESULTS

Exposure to pesticides resulted in significant reduction in the acetylcholinestrase (AChE) activity (P ≤ 0.01). However, groups pretreated with cow urine had improved levels of AChE activity as compared to CPF treated groups.

CONCLUSION

Thus, the present findings clearly show that oral CPF has the propensity to cause significant neurotoxicity in rat brains while cow urine treatment alleviates CPF induced toxicity to a greater extent. In addition, AChE can be used as a potential biomarker of toxicity associated with pesticide exposure.

摘要

引言

有机磷酸酯类农药是用于控制各种害虫和家庭用途的最广泛使用的合成化学品之一。其中毒死蜱(CPF)是全世界包括印度在内使用最广泛的农药。

目的

本研究旨在研究CPF诱导的神经毒性以及牛尿作为一种天然抗氧化剂替代物对减轻CPF神经毒性的调节作用。

设计

为此测定了半数致死剂量(LD50),并选择其四分之一(38毫克/千克体重)用于大鼠治疗。通过ABTS法测定牛尿的抗氧化水平。

结果

接触农药导致乙酰胆碱酯酶(AChE)活性显著降低(P≤0.01)。然而,与CPF处理组相比,用牛尿预处理的组AChE活性水平有所提高。

结论

因此,目前的研究结果清楚地表明,口服CPF有在大鼠脑中引起显著神经毒性的倾向,而牛尿处理在很大程度上减轻了CPF诱导的毒性。此外,AChE可作为与农药接触相关毒性的潜在生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ecc/4987744/0bb3d8508545/40064_2016_3004_Fig1_HTML.jpg

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