The neuroprotective effect of deferoxamine in the hypoxic-ischemic immature mouse brain

Dean P. Sarco, Joseph Becker, Charles Palmer, R. Ann Sheldon, Donna M. Ferriero

Research output: Contribution to journalArticlepeer-review

73 Scopus citations

Abstract

The iron chelator deferoxamine is efficacious in ameliorating hypoxic-ischemic brain injury in some models, perhaps by decreasing oxidative stress. Transgenic copper/zinc superoxide dismutase-1 (SOD1) overexpression in neonatal mice increases brain injury after hypoxia-ischemia compared to non-transgenic wildtype littermates because of increased oxidative stress. A neonatal mouse model of hypoxia-ischemia was used to examine histopathological damage, iron histochemistry and free iron concentration in the brains of SOD1 transgenic and non-transgenic littermates. Deferoxamine significantly decreased injury in non-transgenics compared to controls with a trend toward neuroprotection in the transgenics. There was no difference in free iron concentrations in the brains of SOD1 overexpressors or non-transgenics. Deferoxamine may protect the neonatal brain by a number of anti-oxidant mechanisms including iron chelation, enhancement of stress gene expression, or induction of other factors responsible for neuroprotection. Copyright (C) 2000 Elsevier Science Ireland Ltd.

Original languageEnglish (US)
Pages (from-to)113-116
Number of pages4
JournalNeuroscience letters
Volume282
Issue number1-2
DOIs
StatePublished - Mar 17 2000

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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