ACUTE ACIDOSIS ELEVATES MALONALDEHYDE IN RAT-BRAIN IN-VIVO

Citation
Ah. Waterfall et al., ACUTE ACIDOSIS ELEVATES MALONALDEHYDE IN RAT-BRAIN IN-VIVO, Brain research, 712(1), 1996, pp. 102-106
Citations number
36
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
712
Issue
1
Year of publication
1996
Pages
102 - 106
Database
ISI
SICI code
0006-8993(1996)712:1<102:AAEMIR>2.0.ZU;2-O
Abstract
Oxidative stress in brain tissue was measured experimentally in situ u sing microdialysis to sample the extracellular environment for a lipid peroxidation breakdown product and antioxidants. The extracellular co ncentrations of the lipid peroxidation product malonaldehyde (MDA) and the antioxidants ascorbic acid (AA) and uric acid (UA) were measured in rat cortex and striatum in vivo using microdialysis coupled to HPLC with UV detection. Tissue acidosis following ischaemia and epileptic seizures may contribute to neuronal damage, which may be mediated by r eactive oxygen species. Perfusion of microdialysis probes with acidic artificial cerebrospinal fluid (pH 6) led to a significant increase in the sampled concentration of MDA and the antioxidant ascorbic acid. S imultaneous perfusion of ascorbate (5 mM) with acidic ACSF (pH 6) comp letely attenuated the rise in lipid peroxidation. This study provides in vivo evidence for acidosis induced oxidative stress in brain tissue and an antioxidant action of ascorbate. The methodology described her e can provide direct in vivo information in respect of oxidative stres s in experimental situations. The method could equally be applied to t he assessment of oxidative stress in a number of pathological models n ot necessarily confined to the CNS.