RGD Reference Report - Oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury. - Rat Genome Database

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Oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury.

Authors: Ansari, MA  Roberts, KN  Scheff, SW 
Citation: Ansari MA, etal., Free Radic Biol Med. 2008 Aug 15;45(4):443-52. Epub 2008 May 3.
RGD ID: 2307353
Pubmed: PMID:18501200   (View Abstract at PubMed)
PMCID: PMC2586827   (View Article at PubMed Central)
DOI: DOI:10.1016/j.freeradbiomed.2008.04.038   (Journal Full-text)

Oxidative stress, an imbalance between oxidants and antioxidants, contributes to the pathogenesis of traumatic brain injury (TBI). Oxidative neurodegeneration is a key mediator of exacerbated morphological responses and deficits in behavioral recoveries. The present study assessed early hippocampal sequential imbalance to possibly enhance antioxidant therapy. Young adult male Sprague-Dawley rats were subjected to a unilateral moderate cortical contusion. At various times post-TBI, animals were killed and the hippocampus was analyzed for antioxidants (GSH, GSSG, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, superoxide dismutase, and catalase) and oxidants (acrolein, 4-hydroxynonenal, protein carbonyl, and 3-nitrotyrosine). Synaptic markers (synapsin I, postsynaptic density protein 95, synapse-associated protein 97, growth-associated protein 43) were also analyzed. All values were compared with those for sham-operated animals. Significant time-dependent changes in antioxidants were observed as early as 3 h posttrauma and paralleled increases in oxidants (4-hydroxynonenal, acrolein, and protein carbonyl), with peak values obtained at 24-48 h. Time-dependent changes in synaptic proteins (synapsin I, postsynaptic density protein 95, and synapse-associated protein 97) occurred well after levels of oxidants peaked. These results indicate that depletion of antioxidant systems following trauma could adversely affect synaptic function and plasticity. Early onset of oxidative stress suggests that the initial therapeutic window following TBI appears to be relatively short, and it may be necessary to stagger selective types of antioxidant therapy to target specific oxidative components.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Brain Injuries  ISOG6pd (Rattus norvegicus)2307353; 2307353protein:decreased expression:hippocampusRGD 
Brain Injuries  IEP 2307353protein:decreased expression:hippocampusRGD 

Objects Annotated

Genes (Rattus norvegicus)
G6pd  (glucose-6-phosphate dehydrogenase)

Genes (Mus musculus)
G6pdx  (glucose-6-phosphate dehydrogenase X-linked)

Genes (Homo sapiens)
G6PD  (glucose-6-phosphate dehydrogenase)


Additional Information