| First Author | Sarco DP | Year | 2000 |
| Journal | Neurosci Lett | Volume | 282 |
| Issue | 1-2 | Pages | 113-6 |
| PubMed ID | 10713409 | Mgi Jnum | J:61282 |
| Mgi Id | MGI:1354642 | Doi | 10.1016/s0304-3940(00)00878-8 |
| Citation | Sarco DP, et al. (2000) The neuroprotective effect of deferoxamine in the hypoxic-ischemic immature mouse brain. Neurosci Lett 282(1-2):113-6 |
| abstractText | 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. |
