In submitochondrial particles, NO inhibits complex II-III (but not II) activity.
The inhibition leads to an accumulation of reduced cyt. b, independently on [O2].
NO increases ubisemiquinone EPR signal and, in turn, O2•− and H2O2 production rates.
H2O2 production is also enhanced in coupled mitochondria exposed to NO.
These effects are similar to those reported for the classical inhibitor antimycin.