Regular ArticleOxidative Cellular Damage and the Reduction of APE/Ref-1 Expression after Experimental Traumatic Brain Injury
References (52)
- et al.
Critical evaluation of the use of hydroethidine as a measure of superoxide anion radical
Free Rad. Biol. Med.
(1998) - et al.
DNA strand scission by enzymically generated oxygen radicals
Arch. Biochem. Biophys.
(1981) - et al.
Reactions of oxyl radicals with DNA
Free Rad. Biol. Med.
(1995) - et al.
Going APE over ref-1
Mutat. Res.
(2000) - et al.
Oxidative damage and breakage of DNA in rat brain after transient MCA occlusion
Brain Res.
(1999) - et al.
Antimutagenic role of base-excision repair enzymes upon free radical-induced DNA damage
Mutat. Res.
(1998) - et al.
Carbonyl assays for determination of oxidatively modified proteins
Methods Enzymol.
(1994) - et al.
Single stranded DNA as an immunocytochemical marker for apoptotic change of ischemia in the gerbil hippocampus
Neurosci. Lett.
(1998) - et al.
Early decrease in apurinic/apyrimidinic endonuclease is followed by DNA fragmentation after cold injury-induced brain trauma in mice
Neuroscience
(1999) - et al.
5′-Nicked apurinic/apyrimidinic sites are resistant to beta-elimination by beta-polymerase and are persistent in human cultured cells after oxidative stress
J. Biol. Chem.
(2000)
α-Phenyl-tert-butyl-nitrone inhibits free radical release in brain concussion
Free Rad. Biol. Med.
Parkinson's disease is associated with oxidative damage to cytoplasmic DNA and RNA in substantia nigra neurons
Am. J. Pathol.
The use of salicylate hydroxylation to detect hydroxyl radical generation in ischemic and traumatic brain injury. Reversal by tirilazad mesylate (U-74006F)
Mol. Chem. Neuropathol.
Interaction of human apurinic endonuclease and DNA polymerase beta in the base excision repair pathway
Proc. Natl. Acad. Sci. USA
Superoxide production in rat hippocampal neurons: Selective imaging with hydroethidine
J. Neurosci.
Human apurinic/apyrimidinic endonuclease is processive
Biochemistry
Early detection of DNA strand breaks in the brain after transient focal ischemia: Implications for the role of DNA damage in apoptosis and neuronal cell death
J. Neurochem.
DNA damage and repair in central nervous system injury: National Institute of Neurological Disorders and Stroke workshop summary
Stroke
Oxidative DNA damage precedes DNA fragmentation after experimental stroke in rat brain
FASEB J.
A controlled cortical impact model of traumatic brain injury in the rat
J. Neurosci. Methods.
Mechanism of action of a mammalian DNA repair endonuclease
Biochemistry
APE/Ref-1 responses to ischemia in rat brain
Neuroreport
Transgenic mice with increased Cu/Zn-superoxide dismutase activity: Animal model of dosage effects in Down syndrome
Proc. Natl. Acad. Sci. USA
The 21-aminosteroid U-74389G reduces cerebral superoxide anion concentration following fluid percussion injury of the brain
J. Neurotrauma
Early decrease of apurinic/apyrimidinic endonuclease expression after transient focal cerebral ischemia in mice
J. Cereb. Blood Flow Metab.
Cited by (80)
DNA damage and repair following traumatic brain injury
2021, Neurobiology of DiseaseCitation Excerpt :The resulting mitochondrial dysfunction also promotes ROS formation. In addition, lipid peroxidation, infiltrated macrophages/neutrophils, induction of NADPH oxidases NOX2 and NOX4, and activation of neuronal nitric oxide synthase after TBI leads to increased formation of ROS including superoxide radical, hydroxyl radical, and non-radicals like hydrogen peroxide and singlet oxygen and reactive nitrogen species like nitric oxide (Lewén et al., 2001; Ma et al., 2018). All these molecules lead to extensive DNA damage (Halliwell and Gutteridge, 2015).
Additional functions of selected proteins involved in DNA repair
2020, Free Radical Biology and MedicineCitation Excerpt :In some selected regions of the central nervous system, APE1 is highly expressed [141,142], and reduction of its expression leads to an increase in the rate of apoptosis. This process occurs in the cerebral cortex following compression injury [143], in the hippocampus after hypoxic-ischemic insult [144] and in the spinal cord after ischemia [145]. Increased expression of APE1 in the hippocampus was observed in patients with Alzheimer's disease [146].
The role of DNA damage and repair in toxicity to postmitotic cells caused by cancer therapies
2016, DNA Repair in Cancer Therapy: Molecular Targets and Clinical Applications: Second EditionBase excision repair in the mammalian brain: Implication for age related neurodegeneration
2013, Mechanisms of Ageing and DevelopmentCitation Excerpt :Expression was high throughout the organ during embryonic development, but reduced in all regions post natal except the hippocampus, where mRNA levels remained high in the pyramidal and granule cells at post natal day 21. This early finding was supported by subsequent studies (Edwards et al., 1998a; Gillardon et al., 1997; Lewen et al., 2001; Walton et al., 1997) more focused on characterizing changes in APE1 protein levels after oxidative damage, while offering further insight into protein localization (information collated in Table 2). To summarize these studies, APE1 in the hippocampus can be induced after moderate DNA damage; this protective response is transient and does not occur for longer than 24–36 h.
Oxidative stress, DNA damage, and the telomeric complex as therapeutic targets in acute neurodegeneration
2013, Neurochemistry International