期刊
NEUROBIOLOGY OF DISEASE
卷 8, 期 3, 页码 380-390出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/nbdi.2001.0396
关键词
traumatic brain injury; mice; cellular injury; oxidative stress; DNA repair; DNA oxidation; DNA fragmentation; outcome
资金
- NINDS NIH HHS [NS 14543, NS 82386, NS 38653, NS 25372, NS 36147] Funding Source: Medline
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 expression of 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 after injury. 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.
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