Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Nitric oxide (NO) and its derivatives (reactive nitrogen species) have multiple effects on mitochondria that impact on cell physiology and cell death. Mitochondria may produce and consume NO and NO stimulates mitochondrial biogenesis, apparently via cGMP upregulation of transcriptional factors. NO inhibits mitochondrial respiration via: (A) an acute and reversible inhibition of cytochrome oxidase by NO in competition with O2, and (B) irreversible inhibition of multiple sites by reactive nitrogen species. NO is a potent vasodilator (via cGMP), increasing O2 and respiratory substrate supply to mitochondria. NO stimulates reactive oxygen and nitrogen species production from mitochondria via respiratory inhibition, reaction with ubiquinol and reaction with O2 in the membrane. NO can induce apoptosis, mainly via oxidative stress. NO induces necrosis, mainly via energy depletion. Reactive nitrogen species activation of the mitochondrial permeability transition pore may cause apoptosis or necrosis. NO may protect against mitochondria-mediated cell death by multiple mechanisms.