CEREBRAL PENETRATION INJURY LEADS TO H2O2 GENERATION IN MICRODIALYSISSAMPLES

Citation
Me. Layton et al., CEREBRAL PENETRATION INJURY LEADS TO H2O2 GENERATION IN MICRODIALYSISSAMPLES, Neuroscience letters, 236(2), 1997, pp. 63-66
Citations number
19
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03043940
Volume
236
Issue
2
Year of publication
1997
Pages
63 - 66
Database
ISI
SICI code
0304-3940(1997)236:2<63:CPILTH>2.0.ZU;2-K
Abstract
Delayed tissue damage is proposed to be caused by reactive oxygen spec ies. We investigated the effects of microdialysis probe penetration in to rat piriform cortex on hydrogen peroxide (H2O2) in brain extracellu lar fluid (ECF). H2O2 decreased immediately after probe insertion into the brain, but increased over 300% in samples within minutes after co llection. We assessed H2O2 changes in vitro in microdialysis perfusion media containing various ascorbic acid concentrations and confirmed a scorbic acid is a source of H2O2 We conclude that decreased H2O2 conce ntrations in perfusion media as it passes through the brain reflect an extracellular antioxidant effect, whereas the increase in H2O2 with t ime after sample collection indicates that H2O2 generating substances are present in ECF. Thus, the potential for producing reactive oxygen species in brain ECF exists following penetration injury, especially i f transition metals are released into the neuronal microenvironment. ( C) 1997 Elsevier Science Ireland Ltd.