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Titolo:
Oxidative cellular damage and the reduction of APE/Ref-1 expression after experimental traumatic brain injury
Autore:
Lewen, A; Sugawara, T; Gasche, Y; Fujimura, M; Chan, PH;
Indirizzi:
Stanford Univ, Sch Med, Dept Neurosurg, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 ept Neurosurg, Stanford, CA 94305 USA Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 & Neurol Sci, Stanford, CA 94305 USA Stanford Univ, Sch Med, Neurosci Program, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 rosci Program, Stanford, CA 94305 USA
Titolo Testata:
NEUROBIOLOGY OF DISEASE
fascicolo: 3, volume: 8, anno: 2001,
pagine: 380 - 390
SICI:
0969-9961(200106)8:3<380:OCDATR>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOCAL CEREBRAL-ISCHEMIA; SUPEROXIDE-DISMUTASE PREVENTS; HYDROXYL RADICAL GENERATION; DNA STRAND SCISSION; APURINIC/APYRIMIDINIC ENDONUCLEASE; RAT-BRAIN; TRANSGENIC MICE; EDEMA FORMATION; EARLY DECREASE; MOUSE-BRAIN;
Keywords:
traumatic brain injury; mice; cellular injury; oxidative stress; DNA repair; DNA oxidation; DNA fragmentation; outcome;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Lewen, A Stanford Univ, Sch Med, Dept Neurosurg, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 surg, Stanford, CA 94305 USA
Citazione:
A. Lewen et al., "Oxidative cellular damage and the reduction of APE/Ref-1 expression after experimental traumatic brain injury", NEUROBIOL D, 8(3), 2001, pp. 380-390

Abstract

The DNA repair enzyme, apurinic/apyrimidinic endonuclease (or redox effector factor-1, APE/Ref-1), is involved in base excision repair of apurinic/apyrimidinic sites after oxidative DNA damage. We investigated the expressionof APE/Ref-1 and its relationship to oxidative stress after severe traumatic brain injury produced by controlled cortical impact in normal mice, and in mice over- or underexpressing copper-zinc superoxide dismutase (SOD1TG and SOD1KO, respectively). Oxygen free radical-mediated cellular injury was visualized with 8-hydroxyguanine immunoreactivity as a marker for DNA oxidation, and in situ hydroethidine oxidation as a marker for superoxide production. After trauma there was a reduced expression of APE/Ref-1 in the ipsilateral cortex and hippocampus that correlated with the gene dosage levels of cytosolic superoxide dismutase. The decrease in APE/Ref-1 expression preceded DNA fragmentation. There was also a close correlation between APE/Ref-1 protein levels 4 h after trauma and the volume of the lesion 1 week afterinjury. Our data have demonstrated that reduction of APE/Ref-1 protein levels correlates closely with the level of oxidative stress after traumatic brain injury. We suggest that APE/Ref-1 immunoreactivity is a sensitive marker for oxidative cellular injury. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/05/20 alle ore 13:29:13