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线粒体过氧化氢的形成与抗霉素A介导的对叔丁基过氧化氢诱导的U937细胞死亡的预防存在因果联系。

Mitochondrial formation of hydrogen peroxide is causally linked to the antimycin A-mediated prevention of tert-butylhydroperoxide-induced U937 cell death.

作者信息

Brambilla L, Cantoni O

机构信息

Istituto di Farmacologia e Farmacognosia and Centro di Farmacologia Oncologica Sperimentale, Università di Urbino, Italy.

出版信息

FEBS Lett. 1998 Jul 17;431(2):245-9. doi: 10.1016/s0014-5793(98)00764-9.

Abstract

Antimycin A and 2-heptyl-4-hydroxyquinoline N-oxide (HQNO), both of which bind to the same site of complex III, prevented U937 cell killing promoted by tert-butylhydroperoxide (tB-OOH). This cytoprotection was not directly caused by inhibition of electron transport or reduced formation of tB-OOH-derived toxic species, but rather appeared to be the consequence of a mechanism involving mitochondrial formation of hydrogen peroxide. Ubisemiquinone was most likely the electron donor allowing the formation of superoxides and, as a consequence, of hydrogen peroxide.

摘要

抗霉素A和2-庚基-4-羟基喹啉N-氧化物(HQNO)均与复合物III的同一位点结合,它们可阻止叔丁基过氧化氢(tB-OOH)诱导的U937细胞死亡。这种细胞保护作用并非直接由电子传递抑制或tB-OOH衍生的毒性物质生成减少所致,而是似乎源于一种涉及线粒体过氧化氢形成的机制。泛半醌很可能是允许超氧化物进而过氧化氢形成的电子供体。

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