首页> 外文期刊>Medical science monitor : >Bifenthrin causes neurite retraction in the absence of cell death: A modelfor pesticide associated neurodegeneration.
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Bifenthrin causes neurite retraction in the absence of cell death: A modelfor pesticide associated neurodegeneration.

机译:联苯菊酯在没有细胞死亡的情况下引起神经突退缩:农药相关神经变性的模型。

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Background: Bifenthrin is a synthetic pyrethroid insecticide derivativeof naturally occurring pyrethrins from chrysanthemum flowers. Bifenthrin is considered relatively safeand therefore incorporated as the active ingredient in preparations sold over the counter for householduse. Recent studies have raised concern that chronic exposure to pesticides in the home setting may increasethe risk for neurodegenerative diseases. To address this concer, in the present study, bifenthrin isadded to pre-differentiated PC12 and effect of bifenthrin on the retraction of existing neurites is observeda model for neurodegeneration. Material/Methods: PC12 cells were differentiated with nerve growth factorfor twenty-four hours and then treated with what was determined to be a sublethal dose of bifenthrinfor up to an additional 48 hours. The percent of cells with neurites was assessed at various times beforeand after nerve growth factor treatment. Bifenthrin toxicity was determined using trypan blue exclusion.Results: Bifenthrin was not toxic to PC12 cells at concentrations ranging from 1x10[sup]-10[/sup] M to 1x10[sup]-4[/sup]M. Twenty-four hours after nerve growth factor treatment, a maximum percent of cells had formed neuritesand with a treatment of 1x10[sup]-5[/sup] M bifenthrin, approximately 80% of these neurites retracted in within12 additional hours and almost all neurites had retracted within 48 hours. Trypan exclusion showed thatthese cells were viable. Conclusions: These data show that bifenthrin can stimulate the retraction ofneurites in the absence of frank toxicity.
机译:背景:联苯菊酯是菊科植物菊中天然存在的除虫菊酯的合成拟除虫菊酯杀虫剂衍生物。联苯菊酯被认为是相对安全的,因此作为活性成分掺入了在柜台销售的家用制剂中。最近的研究引起了人们的担忧,即家庭环境中长期接触农药可能会增加神经退行性疾病的风险。为了解决这个问题,在本研究中,联苯菊酯被添加到预分化的PC12中,并且观察到联苯菊酯对现有神经突回缩的作用是神经退行性病变的模型。材料/方法:用神经生长因子分化PC12细胞24小时,然后用确定为亚致死剂量的联苯菊酯处理长达48小时。在神经生长因子治疗之前和之后的不同时间评估具有神经突的细胞的百分比。使用锥虫蓝排除法测定联苯菊酯的毒性。结果:联苯菊酯对PC12细胞无毒,浓度范围为1x10 [-10] M至1x10 [-4] M。神经生长因子治疗后二十四小时,最大百分比的细胞已形成神经突,并用1x10 [sup] -5 [/ sup] M联苯菊酯处理,大约80%的神经突在另外12小时内缩回,几乎所有神经突已在48小时内收回。锥虫排除表明这些细胞是有活力的。结论:这些数据表明联苯菊酯可以在没有明显毒性的情况下刺激神经突的收缩。

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