Reactive Oxygen and Targeted Antioxidant Administration in Endothelial Cell Mitochondria

To better understand the mechanism(s) and site(s) of reactive oxygen species production by endothelial mitochondria we examined ROS production under different substrate and inhibitor conditions

Yunxia O'Malley; Brian D. Fink; Nicolette C. Ross; Thomas E. Prisinzano; William I. Sivitz


Scholarcy highlights

  • We used fluorescent probes and EPR to study the mechanism(s) underlying reactive oxygen species production by endothelial cell mitochondria and the action of mitoquinol, a mitochondria-targeted antioxidant
  • ROS production was markedly inhibited by the complex I inhibitor rotenone
  • As was the case for mitochondria exposed to mitoquinol after isolation, Fig. 7A suggests that succinate-driven H2O2 generation in mitochondria of bovine aortic endothelial cells resulted from reverse electron transport
  • Mitochondria are likely the major site of ROS generation in most cells, little is known about ROS production within endothelial cell mitochondria
  • We report new information concerning the mechanism leading to endothelial ROS production at the mitochondrial level and the means by which targeted quinol/quinone compounds may act on endothelial cell mitochondria
  • We considered that the action of mitoQ on ROS during reverse electron transport might occur through reduction in mitochondrial inner membrane potential and “mild” uncoupling to which reverse electron transport is highly sensitive
  • MitoQ acts in complex I to block reactive oxygen species generated by reverse transport but markedly enhance superoxide production derived from forward electron transport

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