Nitric oxide synthase activity in mitochondria

TL;DR: The data indicate that the redox state of the respiratory chain components regulates H2O2 production and mitochondrial membrane potential modulates NO release, and support the speculation that NO and H2 O2 are a biological signal that reports a high mitochondrial energy charge to the cytosol.

TL;DR: Using functional models for the CcO active site, it is found that NO can protect the respiratory enzyme from other inhibitors such as cyanide, a classic poison.

TL;DR: Results are consistent with the development of cardioprotection during high-altitude acclimatization and provide an experimental model to study the mechanisms involved, which are addressed in the accompanying paper.

TL;DR: How mitochondria harmonize the reversible functions of mtNOS for mitochondrial respiration, its anti-apoptotic actions via S-nitrosation of caspase-3, versus the pro-APoptotic properties of peroxynitrite remains to be fully understood.

TL;DR: The cage mechanism can explain the residual yield of nitrate that appears to be formed even in the presence of high concentrations of all of the scavengers studied to date, since scavengers capture only free HO. and .NO2 and not caged radicals.

TL;DR: Results indicate that nitric oxide is capable of rapidly and reversibly inhibiting the mitochondrial respiratory chain and may be implicated in the cytotoxic effects of Nitric oxide in the CNS and other tissues.

TL;DR: It is assumed, given the monooxygenase-like activity of NOS and the heavy iso- tope labeling studies, that H20 is the ultimate fate of the other oxygen atom.