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首页> 外文期刊>Archives of Toxicology >Cytotoxic effects of hydroxylated fullerenes on isolated rat hepatocytes via mitochondrial dysfunction
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Cytotoxic effects of hydroxylated fullerenes on isolated rat hepatocytes via mitochondrial dysfunction

机译：羟基富勒烯通过线粒体功能障碍对离体大鼠肝细胞的细胞毒性作用

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摘要

The cytotoxic effects of hydroxylated fullerenes, also termed fullerenols or fullerols [C60(OH) n ], which are known nanomaterials and water-soluble fullerene derivatives, were studied in freshly isolated rat hepatocytes. The exposure of hepatocytes to C60(OH)24 caused not only concentration (0–0.25 mM)- and time (0–3 h)-dependent cell death accompanied by the formation of cell blebs, loss of cellular ATP, reduced glutathione (GSH), and protein thiol levels, but also the accumulation of glutathione disulfide and malondialdehyde, indicating lipid peroxidation. Of the other analogues examined, the cytotoxic effects of C60(OH)12 and fullerene C60 at a concentration of 0.125 mM were less than those of C60(OH)24. The loss of mitochondrial membrane potential and generation of oxygen radical species in hepatocytes incubated with C60(OH)24 were greater than those with C60(OH)12 and fullerene C60. In the oxygen consumption of mitochondria isolated from rat liver, the ratios of state-3/state-4 respiration were more markedly decreased by C60(OH)24 and C60(OH)12 compared with C60. In addition, C60(OH)24 and C60(OH)12 resulted in the induction of the mitochondrial permeability transition (MPT), and the effects of C60(OH)12 were less than those of C60(OH)24. Taken collectively, these results indicate that (a) mitochondria are target organelles for fullerenols, which elicit cytotoxicity through mitochondrial failure related to the induction of the MPT, mitochondrial depolarization, and inhibition of ATP synthesis in the early stage and subsequently oxidation of GSH and protein thiols, and lipid peroxidation through oxidative stress at a later stage; and (b) the toxic effects of fullerenols may depend on the number of hydroxyl groups participating in fullerene in rat hepatocytes.
机译：新鲜研究了羟基化富勒烯（也称为富勒烯醇或富勒醇[C 60 （OH） n ]）的细胞毒性作用，这是已知的纳米材料和水溶性富勒烯衍生物。分离的大鼠肝细胞。肝细胞暴露于C 60 （OH） 24 不仅引起浓度（0-0.25 mM）-和时间（0-3 h）依赖性细胞死亡，并伴有细胞泡的形成，细胞ATP的损失，谷胱甘肽（GSH）和蛋白质硫醇水平的降低，以及谷胱甘肽二硫化物和丙二醛的积累，表明脂质过氧化。在检查的其他类似物中，浓度为0.125 mM的C 60 （OH） 12 和富勒烯C 60 的细胞毒性作用小于C 60 （OH） 24 的那些。 C 60 （OH） 24 孵育的肝细胞线粒体膜电位的损失和氧自由基种类的产生要大于C 60 （OH） 12 和富勒烯C 60 。在大鼠肝脏线粒体的耗氧量中，C 60 （OH） 24 和C < sub> 60 （OH） 12 与C 60 的比较。此外，C 60 （OH） 24 和C 60 （OH） 12 导致诱导。线粒体通透性转变（MPT）和C 60 （OH） 12 的作用小于C 60 （OH） 24 。综上所述，这些结果表明：（a）线粒体是富勒烯醇的靶细胞器，其通过与MPT的诱导，线粒体去极化和早期抑制ATP合成以及随后的GSH和蛋白质氧化有关的线粒体衰竭而引起细胞毒性。硫醇和脂质在以后的阶段通过氧化应激而过氧化； （b）富勒烯醇的毒性作用可能取决于参与大鼠肝细胞富勒烯的羟基数目。

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