{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T16:24:24Z","timestamp":1790007864643,"version":"4.0.1"},"reference-count":41,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2007,5,17]],"date-time":"2007-05-17T00:00:00Z","timestamp":1179360000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2007,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Peroxynitrite\u2010mediated oxidative damage has been implicated in brain mitochondrial respiratory dysfunction after traumatic brain injury (TBI), which precedes the onset of neuronal loss. The aim of this study was to investigate the detrimental effects of the peroxynitrite donor SIN\u20101 (3\u2010morpholinosydnonimine) on isolated brain mitochondria and to screen penicillamine, a stoichiometric (1:1) peroxynitrite\u2010scavenging agent, and tempol, a catalytic scavenger of peroxynitrite\u2010derived radicals, as antioxidant mitochondrial protectants. Exposure of the isolated mitochondria to SIN\u20101 caused a significant dose\u2010dependent decrease in the respiratory control ratio and was accompanied by a significant increase in state II respiration, followed by significant decreases (<jats:italic>P<\/jats:italic> &lt; 0.05) in states III and V. These functional alterations occurred together with significant increases in mitochondrial protein carbonyl (PC), lipid peroxidation\u2013related 4\u2010hydroxynonenal (4\u2010HNE), and 3\u2010nitrotyrosine (3\u2010NT) content. Penicillamine hydrochloride (10 \u03bcM) partially but significantly (<jats:italic>P<\/jats:italic> &lt; 0.05) protected against SIN\u20101\u2010induced decreases in states III and V. However, a 2.5 \u03bcM concentration of tempol was able to significantly antagonize a 4\u2010fold molar excess (10 \u03bcM) concentration of SIN\u20101 as effectively as were higher tempol concentrations, consistent with the likelihood that tempol works by a catalytic mechanism. The protection of mitochondrial respiration by penicillamine and tempol occurred in parallel with attenuation of PC, 4\u2010HNE, and 3\u2010NT. These results indicate that SIN\u20101 causes mitochondrial oxidative damage and complex I dysfunction and that antioxidant compounds that target either peroxynitrite or its radicals may be effective mitochondrial protectants in the treatment of neural injury. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.21360","type":"journal-article","created":{"date-parts":[[2007,5,18]],"date-time":"2007-05-18T16:48:45Z","timestamp":1179506925000},"page":"2216-2223","source":"Crossref","is-referenced-by-count":125,"title":["Peroxynitrite\u2010mediated oxidative damage to brain mitochondria: Protective effects of peroxynitrite scavengers"],"prefix":"10.1002","volume":"85","author":[{"given":"Indrapal N.","family":"Singh","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick G.","family":"Sullivan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward 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