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 journalArticle

72 Citations (Scopus)

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

Fingerprint

Deferoxamine
Neuroprotective Agents
Iron
Brain
Brain Injuries
Oxidative Stress
Ischemia
Chelating Agents
Oxidants
Zinc
Copper
Gene Expression
Wounds and Injuries
Superoxide Dismutase-1

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Sarco, Dean P. ; Becker, Joseph ; Palmer, Charles ; Sheldon, R. Ann ; Ferriero, Donna M. / The neuroprotective effect of deferoxamine in the hypoxic-ischemic immature mouse brain. In: Neuroscience letters. 2000 ; Vol. 282, No. 1-2. pp. 113-116.
@article{d55a4717556341d28fdaf0c5588711e2,
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.}",
year = "2000",
month = "3",
day = "17",
doi = "10.1016/S0304-3940(00)00878-8",
language = "English (US)",
volume = "282",
pages = "113--116",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "1-2",

}

The neuroprotective effect of deferoxamine in the hypoxic-ischemic immature mouse brain. / Sarco, Dean P.; Becker, Joseph; Palmer, Charles; Sheldon, R. Ann; Ferriero, Donna M.

In: Neuroscience letters, Vol. 282, No. 1-2, 17.03.2000, p. 113-116.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The neuroprotective effect of deferoxamine in the hypoxic-ischemic immature mouse brain

AU - Sarco, Dean P.

AU - Becker, Joseph

AU - Palmer, Charles

AU - Sheldon, R. Ann

AU - Ferriero, Donna M.

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.

UR - http://www.scopus.com/inward/record.url?scp=0034677852&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034677852&partnerID=8YFLogxK

U2 - 10.1016/S0304-3940(00)00878-8

DO - 10.1016/S0304-3940(00)00878-8

M3 - Article

C2 - 10713409

AN - SCOPUS:0034677852

VL - 282

SP - 113

EP - 116

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 1-2

ER -