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Oxidative cellular damage and the reduction of APE/Ref-1 expression after experimental traumatic brain injury.
Neurobiol Dis. 2001 Jun; 8(3):380-90.ND

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 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.

Authors+Show Affiliations

Department of Neurosurgery, Stanford University School of Medicine, Stanford, California 94305-5487, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11447995

Citation

Lewén, A, et al. "Oxidative Cellular Damage and the Reduction of APE/Ref-1 Expression After Experimental Traumatic Brain Injury." Neurobiology of Disease, vol. 8, no. 3, 2001, pp. 380-90.
Lewén A, Sugawara T, Gasche Y, et al. Oxidative cellular damage and the reduction of APE/Ref-1 expression after experimental traumatic brain injury. Neurobiol Dis. 2001;8(3):380-90.
Lewén, A., Sugawara, T., Gasche, Y., Fujimura, M., & Chan, P. H. (2001). Oxidative cellular damage and the reduction of APE/Ref-1 expression after experimental traumatic brain injury. Neurobiology of Disease, 8(3), 380-90.
Lewén A, et al. Oxidative Cellular Damage and the Reduction of APE/Ref-1 Expression After Experimental Traumatic Brain Injury. Neurobiol Dis. 2001;8(3):380-90. PubMed PMID: 11447995.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative cellular damage and the reduction of APE/Ref-1 expression after experimental traumatic brain injury. AU - Lewén,A, AU - Sugawara,T, AU - Gasche,Y, AU - Fujimura,M, AU - Chan,P H, PY - 2001/7/13/pubmed PY - 2001/8/17/medline PY - 2001/7/13/entrez SP - 380 EP - 90 JF - Neurobiology of disease JO - Neurobiol Dis VL - 8 IS - 3 N2 - 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. SN - 0969-9961 UR - https://www.unboundmedicine.com/medline/citation/11447995/Oxidative_cellular_damage_and_the_reduction_of_APE/Ref_1_expression_after_experimental_traumatic_brain_injury_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0969-9961(01)90396-1 DB - PRIME DP - Unbound Medicine ER -