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• W2085025596 abstract "Peroxynitrite (PN)-mediated mitochondrial dysfunction has been implicated in the secondary injury process after traumatic spinal cord injury (SCI). This study investigated the detrimental effects of the PN donor SIN-1 (3-morpholinosydnonimine) on isolated healthy spinal cord mitochondria and the protective effects of tempol, a catalytic scavenger of PN-derived radicals. A 5 min exposure of the mitochondria to SIN-1 caused a dose-dependent decrease in the respiratory control ratio (RCR) that was accompanied by significant increases in complex I-driven states II and IV respiration rates and decreases in states III and V. These impairments occurred together with an increase in mitochondrial protein 3-nitrotyrosine (3-NT), but not in lipid peroxidation (LP)-related 4-hydroxynonenal (4-HNE). Tempol significantly antagonized the respiratory effects of SIN-1 in parallel with an attenuation of 3-NT levels. These results show that the exogenous PN donor, SIN-1, rapidly causes mitochondrial oxidative damage and complex I dysfunction identical to traumatic spinal cord mitochondrial impairment and that this is mainly due to tyrosine nitration. Consistent with that, the protection of mitochondrial respiratory function by tempol is associated with a decrease in 3-NT levels in mitochondrial proteins also similar to the previously reported antioxidant actions of tempol in traumatically-injured spinal cord mitochondria." @default.
• W2085025596 created "2016-06-24" @default.
• W2085025596 creator A5002997691 @default.
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• W2085025596 date "2009-01-01" @default.
• W2085025596 modified "2023-10-06" @default.
• W2085025596 title "Tempol protection of spinal cord mitochondria from peroxynitrite-induced oxidative damage" @default.
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• W2085025596 doi "https://doi.org/10.1080/10715760902977432" @default.
• W2085025596 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2763567" @default.
• W2085025596 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19513907" @default.
• W2085025596 hasPublicationYear "2009" @default.
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