Suppr超能文献

三氟拉嗪能否保护线粒体免受活性氧诱导的损伤?

Can trifluoperazine protect mitochondria against reactive oxygen species-induced damage?

作者信息

Pereira R de D, Hermes-Lima M

机构信息

Department of Biochemistry, Universidade Estadual Paulista (UNESP), Araraquara, São Paulo, Brazil.

出版信息

Eur J Drug Metab Pharmacokinet. 1996 Oct-Dec;21(4):281-4. doi: 10.1007/BF03189728.

Abstract

Trifluoperazine (TFP) (35 microM) prevents mitochondrial transmembrane potential (delta psi) collapse and swelling induced by 10 microM Ca2+ plus oxyradicals generated from delta-aminolevulinic acid autoxidation. In contrast with EGTA, TFP cannot restore the totally collapsed delta psi. So, TFP might not remove Ca2+ from its 'harmful site', but could impair the ROS-driven cross-linking between membrane-SH proteins. Our data are correlated with the protective uses of TFP against oxidative processes promoted by oxyradicals plus Ca2+.

摘要

三氟拉嗪(TFP)(35微摩尔)可防止由10微摩尔钙离子加δ-氨基乙酰丙酸自氧化产生的氧自由基所诱导的线粒体跨膜电位(δψ)崩溃和肿胀。与乙二醇双四乙酸(EGTA)不同,TFP无法恢复完全崩溃的δψ。因此,TFP可能无法将钙离子从其“有害位点”移除,但可能会损害活性氧驱动的膜-巯基蛋白之间的交联。我们的数据与TFP对氧自由基加钙离子所促进的氧化过程的保护作用相关。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验