Dungel 2015 Free Radic Biol Med

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Dungel P, Perlinger M, Weidinger A, Redl H, Kozlov AV (2015) The cytoprotective effect of nitrite is based on the formation of dinitrosyl iron complexes. Free Radic Biol Med 89:300-10.

» PMID: 26415027

Dungel P, Perlinger M, Weidinger A, Redl H, Kozlov AV (2015) Free Radic Biol Med

Abstract: Nitrite protects various organs from ischemia-reperfusion injury by ameliorating mitochondrial dysfunction. Here we provide evidence that this protection is due to the inhibition of iron-mediated oxidative reactions caused by the release of iron ions upon hypoxia. We show in a model of isolated rat liver mitochondria that upon hypoxia, mitochondria reduce nitrite to nitric oxide (NO) in amounts sufficient to inactivate redox-active iron ions by formation of inactive dinitrosyl iron complexes (DNIC). The scavenging of iron ions in turn prevents the oxidative modification of the outer mitochondrial membrane and the release of cytochrome c during reoxygenation. This action of nitrite protects mitochondrial function. The formation of DNIC with nitrite-derived NO could also be confirmed in an ischemia-reperfusion model in liver tissue. Our data suggest that the formation of DNIC is a key mechanism of nitrite-mediated cytoprotection.

Keywords: Cytochrome c, Cytoprotection, Iron ions, Lipid peroxidation, Mitochondria, Nitrite, Rats

O2k-Network Lab: AT Vienna Kozlov AV


Labels: MiParea: Respiration, mt-Medicine, Pharmacology;toxicology 

Stress:Ischemia-reperfusion, Oxidative stress;RONS  Organism: Rat  Tissue;cell: Liver  Preparation: Isolated mitochondria  Enzyme: Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase 

Coupling state: LEAK, OXPHOS, ET  Pathway: N, S  HRR: Oxygraph-2k 

2016-03