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机构地区:[1]安徽医科大学公共卫生学院,安徽合肥230601 [2]国家知识产权局专利审查协作中心
出 处:《毒理学杂志》2011年第6期427-430,共4页Journal of Toxicology
基 金:安徽省高校优秀青年人才基金(2009SQRZ040);安徽医科大学博士科研启动基金(XJ201016)
摘 要:目的探讨纳米分子筛细胞毒性及其毒性作用机制。方法利用人肺癌A549细胞株48 h培养实验评价不同浓度纳米分子筛细胞毒性,并结合生化指标分析探讨了纳米分子筛氧化应激效应。结果自主合成的纳米分子筛粒径分布均匀,分散相稳定;高浓度纳米分子筛(160 mg/L)明显抑制受试细胞的增殖率(P<0.05),100 mg/L处理组细胞膜受损、通透性增加(P<0.01)。生化指标分析则表明,低于细胞毒性剂量的纳米分子筛明显造成细胞内超氧化物歧化酶(SOD)活性和还原性谷胱甘肽(GSH)含量的降低,显示氧化应激效应。结论氧化应激效应可能是纳米分子筛细胞毒性的作用机制,而且显示出较细胞损伤更为敏感。Objective The cytotoxicity of nanocrystalline silicalite and the potential toxicological mechanism were investigated. Methods A549 human lung cancer cell line was treated with different dosages of nano-silicalite synthesized in this work. "Cellular damage then was evaluated by microscopy after 48 h exposure as well as the biochemical assay of superoxide dismutase (SOD) activities and the reduced glutathione (GSH) contents. Results The nano-silicalite exhibited a narrow diameter and a homogeneous dispersion in aqueous solutions. After 48 h exposure, A549 cell growth were significantly inhibited by nano-siliealite at high concentration (160 rag/L) as well as the cell membrane was disrupted at 100 mg/L dose. In addition, significant decrease in SOD activities and GSH contents were observed in a dose-dependent manner. Conclusion A549 cell could be disrupted by nanocrystalline silicalite, in which the mechanism may attribute to the oxidative stress.
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