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

doi:10.1016/S0304-3940(00)00878-8

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 journal › Article › peer-review

84 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 language	English (US)
Pages (from-to)	113-116
Number of pages	4
Journal	Neuroscience letters
Volume	282
Issue number	1-2
DOIs	https://doi.org/10.1016/S0304-3940(00)00878-8
State	Published - Mar 17 2000

All Science Journal Classification (ASJC) codes

General Neuroscience

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10.1016/S0304-3940(00)00878-8

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title = "The neuroprotective effect of deferoxamine in the hypoxic-ischemic immature mouse brain",

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.",

author = "Sarco, {Dean P.} and Joseph Becker and Charles Palmer and Sheldon, {R. Ann} and Ferriero, {Donna M.}",

note = "Funding Information: D.P.S .is a recipient of the American Heart Association Student Fellowship and the Genentech Foundation Research Fellowship. This research was also supported by NIH grant NS33997 to D.M.F. and HD31704 to C.P. We wish to acknowledge Jessica L. Derstine and Nicholas King for technical assistance in brain iron measurements.",

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AU - Ferriero, Donna M.

N1 - Funding Information: D.P.S .is a recipient of the American Heart Association Student Fellowship and the Genentech Foundation Research Fellowship. This research was also supported by NIH grant NS33997 to D.M.F. and HD31704 to C.P. We wish to acknowledge Jessica L. Derstine and Nicholas King for technical assistance in brain iron measurements.

PY - 2000/3/17

Y1 - 2000/3/17

N2 - 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.

AB - 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.

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

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