Ascorbic acid and focal cerebral ischaemia in a primate model

Neuronal cell damage following ischaemia is postulated to be due to free radical induced lipid peroxidation, and ascorbic acid is supposedly an important non-enzymatic scavenger of such free radicals. This study was undertaken to evaluate the protective effect of ascorbic acid on the brain in a primate model after focal cerebral ischaemia. Consumption of ascorbic acid in the monkey brain following ischaemia and its effect on macroscopic infarct size as demonstrated by 2, 3, 5, Triphenyl tetrazolium chloride (TTC) staining were used as parameters. The monkeys in the treated group were given 1 gram ascorbic acid parenterally every day for six days. The mean level of total ascorbic acid in right basal ganglia was 35.1±4.2 μg/mg of protein in the treated group as opposed to 22.9±2.1 μg/mg of protein in the nontreated group both before ischaemia. After right middle cerebral artery occlusion to produce focal cerebral ischaemia, the total ascorbic acid in the right basal ganglia 2 hours post ischaemia was 13.3±3.1 μg/mg of protein in the treated group as opposed to 9±1.6 μg/mg of protein in the untreated group. The average consumption of total ascorbic acid was 21.8 μg/mg of protein in the treated group and 13.9 μg/mg of protein in the nontreated group. Macroscopic infarct size as determined by TTC staining in the right cerebral hemisphere was 11.7±6.9 in treated group whereas it was 24.4±4.4 (expressed as percentage of right hemisphere) in the non-treated group. There was significant reduction in the size of the infarct in the treated group. A short course of mega-dose Ascorbic acid therapy was found to significantly decrease the macroscopic infarct size. Pretreatment with ascorbic acid enhanced its storage and utilization during ischaemia resulting in its protective effect.