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Ascorbic acid and focal cerebral ischaemia in a primate model
A Ranjan1, D Theodore, R P Haran
1Department of Neurological Sciences, Christian Medical College Hospital, Vellore, India.
Acta Neurochirurgica
|January 1, 1993
Summary
Ascorbic acid (vitamin C) protects the primate brain from ischemic damage by reducing free radical-induced cell injury. This study demonstrates ascorbic acid
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Neuronal cell damage after ischemia is linked to free radical-induced lipid peroxidation.
- Ascorbic acid is a key non-enzymatic scavenger of free radicals.
Purpose of the Study:
- To evaluate the protective effect of ascorbic acid on the brain in a primate model following focal cerebral ischemia.
- To assess ascorbic acid consumption and infarct size after induced ischemia.
Main Methods:
- Primate model of focal cerebral ischemia induced by middle cerebral artery occlusion.
- Administration of 1 gram ascorbic acid parenterally daily for six days to the treated group.
- Measurement of total ascorbic acid levels in the basal ganglia and infarct size using 2, 3, 5, Triphenyl tetrazolium chloride (TTC) staining.
Main Results:
- Treated group showed significantly higher ascorbic acid levels in the basal ganglia both before and after ischemia compared to the untreated group.
- Average ascorbic acid consumption was higher in the treated group.
- Macroscopic infarct size was significantly reduced in the ascorbic acid-treated group (11.7%) compared to the untreated group (24.4%).
Conclusions:
- Ascorbic acid administration demonstrates a significant protective effect against focal cerebral ischemia in a primate model.
- Ascorbic acid effectively scavenges free radicals, mitigating neuronal damage and reducing infarct volume.
- These findings support the therapeutic potential of ascorbic acid in managing ischemic brain injury.