This finding suggests a potential usefulness of antioxidants for treating diabetes and provides further support for the implication of free radicals in beta-cell dysfunction in diabetes. The treatment was repeated every three weeks until progression. Response to therapy was evaluated after 2 and 4 treatment courses. Adverse events were judged as related to the drug 5-FU and consisted of liver toxicity. 128, Iss 8, PP 1754-1760 A study examined the effect of melatonin, a potent antioxidant, and deprenyl, a neuroprotectant, as inhibitors of use of an excitotoxic compound, quinolinic acid.
Quinolinic acid induces damage to the hippocampus of the brain.
Quinolinic acid increased the formation of lipid peroxidation products from hippocampal tissue and this effect was prevented by melatonin. Deprenyl also prevented quinolinic acid- induced damage at a dose of 50 nmols but not at 10 nmols. The results suggest that quinolinic acid-induced neuronal damage can be prevented by melatonin and deprenyl, which can act as a potent free radical scavenger and can increase the activity of endogenous antioxidant enzymes. This suggests that free radical formation contributes significantly to quinolinic acid-induced damage in vivo. The risk of stroke is reduced by surgery in those with high-grade stenosis.