Inhibition of transition metal ion-catalysed ascorbate oxidation and lipid peroxidation by allopurinol and oxypurinol

• Published in: Biochemical pharmacology Vol. 40; no. 4; p. 803
• Main Authors: Ko, K M, Godin, D V
• Format: Journal Article
• Language: English
• Published: England 15.08.1990
• Subjects: Allopurinol - pharmacology; Ascorbic Acid - metabolism; Butylated Hydroxytoluene - pharmacology; Copper - pharmacology; Edetic Acid - pharmacology; Erythrocyte Membrane - metabolism; Humans; Iron - pharmacology; Lipid Peroxidation - drug effects; Membrane Lipids - metabolism; Oxidation-Reduction; Oxypurinol - pharmacology; Pyrimidines - pharmacology; Uric Acid - pharmacology
• ISSN: 0006-2952
• DOI: 10.1016/0006-2952(90)90319-G

Allopurinol and its metabolite oxypurinol inhibited basal oxidation of ascorbate and exerted comparable concentration-dependent inhibitory effects on the oxidation of ascorbate catalysed by cupric ion, but the stimulation produced by ferric ion was affected minimally. UV spectral analysis suggested the formation of an allopurinol-ascorbate-copper ion complex. The oxidation of erythrocyte membrane lipids by ferric ion and cupric ion-t-butylhydroperoxide was also inhibited by allopurinol and oxypurinol, by the metal chelators EDTA and uric acid, and by the antioxidant butylated hydroxytoluene. The metal chelating actions of allopurinol and oxypurinol may be relevant to their protective actions against ischemia/reperfusion injury.