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Neurosci Lett. 2000 Mar 17;282(1-2):113-6.

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

Author information

1
Neonatal Brain Disorders Laboratory, Departments of Neurology, University of California-San Francisco, San Francisco, USA.

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.

PMID:
10713409
DOI:
10.1016/s0304-3940(00)00878-8
[Indexed for MEDLINE]

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