Brambilla L, Cantoni O
Istituto di Farmacologia e Farmacognosia and Centro di Farmacologia Oncologica Sperimentale, Università di Urbino, Italy.
FEBS Lett. 1998 Jul 17;431(2):245-9. doi: 10.1016/s0014-5793(98)00764-9.
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.
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。
