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Impairment of the ability of the injured aged brain in elevating urate and ascorbate.
- Moor E, Shohami E, Kanevsky E, Grigoriadis N, Symeonidou C, Kohen R
Exp Gerontol. 2006 Mar;41(3):303-11. Epub 2006 Feb 3.
Urate
and ascorbate play a major role
in the defense mechanism
of the brain against oxidative damage induced by traumatic
brain injury.
The severity and extent of brain damage are known to increase with age. This may be due to different basal levels of endogenous antioxidants,
and/or to impaired ability of the old brain to recruit
and elevate the levels of antioxidants
following injury. To investigate this hypothesis, we measured basal ascorbate and urate
levels in the hippocampus, using microdialysis
in young, adults and old rats, and performed closed head injury
(CHI)
in young (5-6 weeks) and old rats (19-20 months). Basal ascorbate, but not urate
levels in old rats were significantly lower than in the adults. The ability of the old rats to increase ascorbate levels after CHI
was significantly lower than that of the young ones, as indicated by lower levels of ascorbate and urate
in the dialysate of old rats. This lower level of antioxidant
mobilization in the old brain may explain the extended damage found in histology.
Evaluation
of hippocampal
cell loss (p<0.05) and axonal degeneration
in the corpus callosum
showed more extensive damage in old as compared to young rats (chi(2)=4.25; p<0.05). These findings shed
more light on the susceptibility of old rat brain to CHI-induced oxidative damage.
This abstract at PubMed.