title: The interactions between nitric oxide and brain nerve terminals as studied by electron paramagnetic resonance.
abstract: It has been proposed that nitric oxide (NO) toxicity is due to damage to mitochondrial iron-sulfur centers, resulting in inhibition of mitochondrial respiration and the appearance of an EPR-detectable (g = 2.04) iron-sulfur dinitrosyl complex - Fe(RS)2(NO)2. We show that the addition of nitroprusside (an NO and NO+ donor) to rat brain synaptosomes generates large (> 30 microM) concentrations of EPR-detectable iron-sulfur-dinitrosyl complexes. However, there was no correlation between the size of the g = 2.04 EPR signal and the inhibition of synaptosomal respiration. No significant loss of intensity was seen from the mitochondrial iron-sulfur protein EPR signals. The results are consistent with previous data demonstrating that cytochrome oxidase, not iron-sulfur enzymes, is the primary target for NO inhibition of brain cell respiration (Brown, G.C. and Cooper, C.E. (1994) FEBS Lett. 356, 295-298).
authors.affiliation: Department of Paediatrics, University College London Medical School, Rayne Institute, UK.
authors.forename: C E
authors.initials: CE
authors.lastname: Cooper
authors.forename: G C
authors.initials: GC
authors.lastname: Brown
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000648:ultrastructure*; D004578:Electron Spin Resonance Spectroscopy; D007506:Iron-Sulfur Proteins / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009411:Nerve Endings / Q000187:drug effects / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism
chemical_list: D007506:Iron-Sulfur Proteins; D009599:Nitroprusside; D009569:Nitric Oxide