Related Experiment Videos
Acute acidosis elevates malonaldehyde in rat brain in vivo
A H Waterfall1, G Singh, J R Fry
1Department of Physiology and Pharmacology, Medical School, Queens Medical Centre, Nottingham, UK.
Brain Research
|March 11, 1996
Summary
Acidosis induces oxidative stress in brain tissue, increasing lipid peroxidation. Ascorbic acid (AA) acts as an antioxidant, mitigating this damage in vivo. This study highlights a novel method for assessing brain oxidative stress.
Area of Science:
- Neuroscience
- Biochemistry
- Physiology
Background:
- Oxidative stress in brain tissue is implicated in neuronal damage.
- Acidosis, following ischemia or seizures, may mediate this damage via reactive oxygen species.
Purpose of the Study:
- To investigate the link between acidosis and oxidative stress in brain tissue in vivo.
- To evaluate the antioxidant capacity of ascorbic acid (AA) in mitigating acidosis-induced oxidative stress.
Main Methods:
- In vivo microdialysis was used to sample extracellular fluid in rat cortex and striatum.
- HPLC with UV detection measured malonaldehyde (MDA) and antioxidants (AA, uric acid).
- Perfusion with acidic artificial cerebrospinal fluid (ACSF) and AA was performed.
Main Results:
- Acidic ACSF (pH 6) significantly increased MDA and AA concentrations.
- Simultaneous perfusion with AA (5 mM) completely prevented the rise in lipid peroxidation.
- This demonstrates in vivo evidence of acidosis-induced oxidative stress and AA's antioxidant effect.
Conclusions:
- Acidosis is a significant contributor to oxidative stress in brain tissue.
- Ascorbic acid effectively attenuates acidosis-induced lipid peroxidation in vivo.
- The described microdialysis methodology offers a valuable tool for real-time assessment of oxidative stress in various experimental models.