Permethrin is a synthetic insecticide, extensively used in pest control. Exposures to permethrin have been attributed to increased cell death. The mechanism for its toxicity is still not clear. Hence, in the present study we determined the molecular mechanism associated with permethrin induce cytotoxicity. Rat splenocytes were incubated with increasing concentration of permethrin (0-39 ug/Ml) for 6 to 24 h. Cytotoxic effect of permethrin was evaluated by MTT assay. To assess the mechanism of cytotoxicity, different biochemical indices of cell death, namely annexin V binding assay, DNA fragmentation assay, and levels of caspase 3 were analyzed. To evaluate the oxidative stress, glutathione depletion and melondialdehyde levels were analyzed. MTT assay revealed that permethrin induces cytotoxicity in dose-dependent way. In annexin-V binding assay, above 7.8 µg/mL concentration, significant necrosis of cells was noticed and consistent with DNA fragmentation assay. A significant dose and time dependent depletion of cellular glutathione (GSH) and increased MDA levels were observed and consistent with the percentage of cells undergoing apoptosis. Co administration of N-acetycysteine mitigates permethrin- induced apoptosis, showing the role of oxidative stress in apoptosis induction. The present study demonstrated the role of oxidative stress in permethrin-induced cytotoxicity in rat splenocytes in vitro.

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苄氯菊酯诱导的大鼠脾细胞的细胞毒性：N-乙酰半胱氨酸的保护作用

氯菊酯是一种合成杀虫剂，广泛用于害虫防治。氯菊酯的暴露已被归因于细胞死亡的增加。其毒性机理尚不清楚。因此，在本研究中，我们确定了与苄氯菊酯诱导细胞毒性有关的分子机制。将大鼠脾细胞与浓度递增的苄氯菊酯（0-39 ug / Ml）孵育6至24小时。通过MTT分析评价苄氯菊酯的细胞毒性作用。为了评估细胞毒性的机理，分析了细胞死亡的不同生化指标，即膜联蛋白V结合测定，DNA片段化测定和胱天蛋白酶3的水平。为了评估氧化应激，分析了谷胱甘肽耗竭和乙二醛水平。MTT分析表明苄氯菊酯以剂量依赖性方式诱导细胞毒性。在膜联蛋白-V结合试验中 浓度超过7.8 µg / mL时，注意到细胞明显坏死，与DNA片段分析一致。观察到明显的剂量和时间依赖性的细胞谷胱甘肽（GSH）消耗和MDA水平升高，这与经历凋亡的细胞百分比一致。N-乙酰半胱氨酸的共同给药减轻了氯菊酯诱导的细胞凋亡，显示了氧化应激在细胞凋亡诱导中的作用。本研究证明了氧化应激在氯菊酯诱导的大鼠脾细胞毒性中的作用 N-乙酰半胱氨酸的共同给药减轻了氯菊酯诱导的细胞凋亡，显示了氧化应激在细胞凋亡诱导中的作用。本研究表明氧化应激在氯菊酯诱导的大鼠脾细胞毒性中的作用 N-乙酰半胱氨酸的共同给药减轻了氯菊酯诱导的细胞凋亡，显示了氧化应激在细胞凋亡诱导中的作用。本研究表明氧化应激在氯菊酯诱导的大鼠脾细胞毒性中的作用体外。