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首页> 外文期刊>RSC Advances >Role of membrane disturbance and oxidative stress in the mode of action underlying the toxicity of differently charged polystyrene nanoparticles
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Role of membrane disturbance and oxidative stress in the mode of action underlying the toxicity of differently charged polystyrene nanoparticles

机译：膜扰动和氧化应激在不同电荷聚苯乙烯纳米粒子毒性下面的作用中的作用

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Surface charge is often hypothesized to influence toxicity of nanoparticles (NPs) including polymeric nanoparticles (PNPs) while oxidative stress is considered to be an important mode of action (MOA) for such toxicity. In order to investigate the role of membrane disturbance and oxidative stress in the MOA of PNPs, the cytotoxicity and a range of related cellular endpoints induced by monodisperse, fluorescent, cationic and anionic polystyrene nanoparticles (PSNPs) of 50 and 100 nm sizes were investigated in vitro in macrophage NR8383 cells. Only amine-terminated cationic PSNPs exhibited cytotoxicity which was accompanied by induction of intracellular reactive oxygen species (ROS), increased levels of cytoplasmic free calcium, a reduced phagocytic index, a reduced mitochondrial membrane potential (Δ Ψ _(m) ) and a decreased intracellular ATP content with the effects being more pronounced for 50 nm than 100 nm PSNPs. Both cationic and anionic PSNPs were found to increase the roughness of the cell membrane with the effect being more profound for cationic PSNPs. The pattern of protection by cellular antioxidants against the effects induced by positive PSNPs was similar to the pattern of protection against effects induced by the mitochondrial electron transport disrupting agent 2,4-dinitrophenol (DNP) and dissimilar to that for protection against the model compound for oxidative stress, i.e. hydrogen peroxide (H _(2) O _(2) ). Surface charge influences the cellular interaction for NPs. The results collectively indicated that membrane interaction, and disturbance of the mitochondrial electronic transport chain (ETC) may represent a principal mechanism of toxicity for cationic PSNPs resulting in ROS production and oxidative stress as secondary effects.
机译：通常假设表面电荷以影响包括聚合物纳米颗粒（PNP）的纳米颗粒（NP）的毒性，而氧化应激被认为是这种毒性的重要作用方式（MOA）。为了探讨膜扰动和氧化应激在PNP的MOA中的作用，研究了通过单分散，荧光，阳离子和阴离子聚苯乙烯纳米颗粒（PSNP）为50和100nm尺寸的细胞毒性和一系列相关细胞终点体外巨噬细胞NR8383细胞。只有胺封端的阳离子Psnps表现出细胞毒性，伴随着细胞内反应性氧物质（ROS）的诱导，细胞质自由钙水平增加，降低的吞噬指数，降低的线粒体膜电位（Δ_（m））和减少细胞内ATP含量与100nm psnps更明显的效果更明显。发现阳离子和阴离子Psnps都增加了细胞膜的粗糙度，阳离子psnps的效果更深刻。细胞抗氧化剂免受阳性PSNP诱导的效果的保护类似于由线粒体电子传输破坏剂2,4-二硝基苯酚（DNP）诱导的效果的保护模式，以及用于保护模型化合物的保护氧化应激，即过氧化氢（H _（2）O _（2））。表面电荷影响NPS的细胞相互作用。结果集体表明，线粒体电子传输链（ETC）的膜相互作用和扰动可以代表阳离子PSNP的主要毒性机制，导致ROS产生和氧化应激作为二次效果。

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