Cerebral penetration injury leads to H2O2 generation in microdialysis samples

• Published in: Neuroscience letters 1997-10, Vol.236 (2), p.63-66
• Main Authors: LAYTON, M. E, PAZDERNIK, T. L, SAMSON, F. E
• Format: Article
• Language: English
• Subjects: Animals; Ascorbic Acid - pharmacology; Biochemistry and metabolism; Biological and medical sciences; Brain Injuries - metabolism; Central nervous system; Extracellular Space - physiology; Fundamental and applied biological sciences. Psychology; Hydrogen Peroxide - metabolism; Male; Microdialysis; Rats; Rats, Wistar; Time Factors; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(97)00765-9

Delayed tissue damage is proposed to be caused by reactive oxygen species. We investigated the effects of microdialysis probe penetration into rat piriform cortex on hydrogen peroxide (H2O2) in brain extracellular fluid (ECF). H2O2 decreased immediately after probe insertion into the brain, but increased over 300% in samples within minutes after collection. We assessed H2O2 changes in vitro in microdialysis perfusion media containing various ascorbic acid concentrations and confirmed ascorbic acid is a source of H2O2. We conclude that decreased H2O2 concentrations in perfusion media as it passes through the brain reflect an extracellular antioxidant effect, whereas the increase in H2O2 with time 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 if transition metals are released into the neuronal microenvironment.