Chloromethyltetramethylrosamine (Mitotracker Orange) induces the mitochondrial permeability transition and inhibits respiratory complex I. Implications for the mechanism of cytochrome c release.

摘要: We have investigated the interactions with isolated mitochondria and intact cells of chloromethyltetramethylrosamine (CMTMRos), a probe (Mitotracker Orange) that is increasingly used to monitor mitochondrial membrane potential (Deltapsi(m)) in situ. CMTMRos binds undergoes large fluorescence quenching. Most binding energy-independent can be substantially reduced by sulfhydryl reagents. A smaller fraction able redistribute across inner response potential, further Within minutes, however, this energy-dependent quenching spontaneously reverts same level obtained treating uncoupler carbonylcyanide-p-trifluoromethoxyphenyl hydrazone. show event depends on inhibition respiratory chain at complex I induction permeability transition pore CMTMRos, concomitant depolarization, swelling, release cytochrome c. After staining depolarization situ protonophores accompanied changes range between small undetectable, depending concentration. lasting decrease cellular associated only results from treatment thiol reagents, suggesting living largely occurs SH groups via chloromethyl moiety irrespective magnitude Deltapsi(m). Induction precludes use as reliable Deltapsi(m) demands reassessment conclusion c occur without and/or onset transition.