期刊
BIOMEDICAL RESEARCH-TOKYO
卷 22, 期 4, 页码 183-186出版社
BIOMEDICAL RESEARCH PRESS LTD
DOI: 10.2220/biomedres.22.183
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Maltol (3-hydroxy-2-methyl-4-pyrone) inhibited iron-mediated lipid peroxidation, determined as the formation of thiobarbituric acid-reactive substances, but dimethylpyrone, an analogue of maltol showed no effect on the formation of lipid peroxides. NADP-isocitrate dehydrogenase, a principal enzyme generating reduced NADP, was protected by maltol but not by dimethylpyrone from the ferrous ion-mediated inactivation. Protection of NADP-isocitrate dehydrogenase can enhance the supply of NADPH required for the regeneration of reduced glutathione for scavenging reactive oxygen species. Antioxidant properties of maltol were closely related to the enhanced oxidation of ferrous ion as a prooxidant, and can be explained by the electron-deficient nature of 3-hydroxypyrone ring.
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