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Dehydroascorbic acid is an oxidized form of ascorbic acid (Item No. 14656).1 It is obtained through the diet or formed via oxidation of ascorbic acid in the gut and can also be reduced back to ascorbic acid in various cell types. Dehydroascorbic acid (0.5 and 1 mM) inhibits hydrogen peroxide-induced cell death in murine astrocytes by approximately 74 and 83%, respectively.2 It also increases glutathione peroxidase (GPX) and glutathione reductase activity and inhibits production of reactive oxygen species (ROS) in hydrogen peroxide-treated astrocytes when used at a concentration of 1 mM. Dehydroascorbic acid (40 and 250 mg/kg) increases cerebral blood flow and reduces infarct volume and mortality in a mouse model of cerebral ischemia-reperfusion injury induced by transient middle cerebral artery occlusion (MCAO) when administered prior to ischemia.3 It also reduces infarct volume in a permanent MCAO mouse model when administered pre- or post-ischemia at doses of 250 and 500 mg/kg, respectively.
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1. The physiological role of dehydroascorbic acid. FEBS Lett. 527(1-3), 5-9 (2002).
2. Dehydroascorbic acid prevents oxidative cell death through a glutathione pathway in primary astrocytes. J. Neurosci. Res. 79(5), 670-679 (2005).
3. Dehydroascorbic acid, a blood-