Oxypurinol inhibits free radical release from the cerebral cortex of closed head injured rats

Traumatic brain injury (TBI) is a significant cause of mortality and morbidity. Although the sequence of events underlying the resultant neuronal loss is still poorly understood, there are indications that oxygen-free radical generation is critically involved. Free radical generation in the cerebral...

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Veröffentlicht in:Neuroscience letters 1993-11, Vol.162 (1), p.117-120
Hauptverfasser: Sen, Souvik, Goldman, Harold, Morehead, Marilyn, Murphy, Sharon, Phillis, John W.
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Sprache:eng
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Zusammenfassung:Traumatic brain injury (TBI) is a significant cause of mortality and morbidity. Although the sequence of events underlying the resultant neuronal loss is still poorly understood, there are indications that oxygen-free radical generation is critically involved. Free radical generation in the cerebral cortex of closed head injury rats was monitored by measuring free radical release into cortical superfusates containing the spin trap agent 4-pyridyl-1-oxide- N-tert-butylnitrone (POBN, 100 mM). ESR analysis of the superfusates revealed six line spectra ( α N = 15.4 G and α H β = 2.5 G) characteristic of POBN-OH adducts. Administration of oxypurinol (40 mg/kg) 15 min prior to TBI prevented the formation of these radical adducts.
ISSN:0304-3940
1872-7972
DOI:10.1016/0304-3940(93)90574-5