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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.

DOI:10.1007/BF03189728
PMID:9074891
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。

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本文引用的文献

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The participation of reactive oxygen species and protein thiols in the mechanism of mitochondrial inner membrane permeabilization by calcium plus prooxidants.活性氧和蛋白质巯基在钙加促氧化剂导致线粒体内膜通透性改变机制中的作用。
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Membrane protein thiol cross-linking associated with the permeabilization of the inner mitochondrial membrane by Ca2+ plus prooxidants.膜蛋白硫醇交联与Ca2+加促氧化剂引起的线粒体内膜通透性改变相关。
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