...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of applied toxicology >Comparative effects of sulfhydryl compounds on target organellae, nuclei and mitochondria, of hydroxylated fullerene-induced cytotoxicity in isolated rat hepatocytes
【24h】

Comparative effects of sulfhydryl compounds on target organellae, nuclei and mitochondria, of hydroxylated fullerene-induced cytotoxicity in isolated rat hepatocytes

机译：巯基化合物对靶细胞细胞，核和线粒体，羟基化富勒烯诱导的细胞毒性在分离的大鼠肝细胞中的比较作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

DNA damage and cytotoxicity induced by a hydroxylated fullerene [C-60(OH)(24)], which is a spherical nanomaterial and/or a water-soluble fullerene derivative, and their protection by sulfhydryl compounds were studied in freshly isolated rat hepatocytes. The exposure of hepatocytes to C-60(OH)(24) at a concentration of 50M caused time (0 to 3h)-dependent cell death accompanied by the formation of cell surface blebs, the loss of cellular levels of ATP and reduced glutathione, accumulation of glutathione disulfide, and induction of DNA fragmentation assayed using alkali single-cell agarose-gel electrophoresis. C-60(OH)(24)-induced cytotoxicity was effectively prevented by pretreatment with sulfhydryl compounds. N-acetyl-L-cysteine (NAC), L-cysteine and L-methionine, at a concentration of 2.5mM, ameliorated cell death, accompanied by a decrease in cellular ATP levels, formation of cell surface blebs, induction of reactive oxygen species (ROS) and loss of mitochondrial membrane potential caused by C-60(OH)(24). In addition, DNA fragmentation caused by C-60(OH)(24) was also inhibited by NAC, whereas an antioxidant ascorbic acid did not affect C-60(OH)(24)-induced cell death and DNA damage in rat hepatocytes. Taken collectively, these results indicate that incubation of rat hepatocytes with C-60(OH)(24) elicits DNA damage, suggesting that nuclei as well as mitochondria are target sites of the hydroxylated fullerene; and induction of DNA damage and oxidative stress is ameliorated by an increase in cellular GSH levels, suggesting that the onset of toxic effects may be partially attributable to a thiol redox-state imbalance caused by C-60(OH)(24). Copyright (c) 2015 John Wiley & Sons, Ltd.
机译：用羟基化富勒烯[C-60（OH）（24）]诱导的DNA损伤和细胞毒性，其是球形纳米材料和/或水溶性富勒烯衍生物，并在新鲜分离的大鼠肝细胞中研究了巯基化合物的保护。肝细胞暴露于C-60（OH）（24）的浓度为50m的诱发时间（0至3H） - 依赖性细胞死亡伴随着细胞表面填充的形成，损失ATP和谷胱甘肽的细胞水平丧失，使用碱单细胞琼脂糖 - 凝胶电泳测定谷胱甘肽二硫化物的积累和DNA碎片的诱导。通过用巯基化合物预处理有效地防治C-60（OH）（24）诱导的细胞毒性。 N-乙酰基-1-半胱氨酸（NAC），L-半胱氨酸和L-蛋氨酸，浓度为2.5mm，改善细胞死亡，伴有细胞ATP水平的减少，形成细胞表面填充，诱导反应性氧物种（ROS）和由C-60（OH）（24）引起的线粒体膜电位的丧失。此外，由C-60（OH）（24）引起的DNA片段化也被NAC抑制，而抗氧化剂抗坏血酸不影响大鼠肝细胞的C-60（OH）（24）次诱导的细胞死亡和DNA损伤。这些结果集体表明，用C-60（OH）（24）的大鼠肝细胞引发DNA损伤，表明核以及线粒体是羟基化富勒烯的靶位点;通过细胞GSH水平的增加改善DNA损伤和氧化应激的诱导，表明毒性效应的发作可以部分地应对由C-60（OH）（24）引起的硫醇氧化氢状态不平衡。版权所有（c）2015 John Wiley＆Sons，Ltd。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号