Dehydroascorbic acid

Dehydroascorbic acid is an oxidized form of vitamin C that can cross the blood-brain barrier (BBB). Dehydroascorbic acid clears cytotoxic reactive oxygen species (ROS) produced after ischemic stroke by converting to ascorbic acid (AA), thereby reducing neuronal and glial cell damage and stabilizing cerebral microvascular NO signaling to maintain perfusion in the ischemic area. Dehydroascorbic acid can be used in research on ischemic stroke^[1][2]. In Vitro:Neuronal injury in ischemic stroke is partly mediated by cytotoxic reactive oxygen species. Although the antioxidant ascorbic acid (AA) or vitamin C does not penetrate the blood-brain barrier (BBB), its oxidized form, dehydroascorbic acid (DHA), enters the brain by means of facilitative transport^[1]. In Vivo:Dehydroascorbic acid (40, 250 mg/kg, intravenous injection, single dose) dose-dependently improves cerebral blood flow, reduces neurological deficit scores, and decreases mortality in C57BL6J mice models of transient focal cerebral ischemia (reperfusion) and permanent focal cerebral ischemia (non-reperfusion)^[2].
Dehydroascorbic acid (250, 500 mg/kg, intravenous injection, single dose) dose-dependently reduces infarct volume, improves neurological function, increases cerebral blood flow at 24 hours, and decreases mortality in C57BL6J mice with permanent focal cerebral ischemia (administered 3 hours after ischemia)^[2].
In C57BL6J mouse models of cerebral ischemia, dehydroascorbic acid (intravenous injection, single dose) can penetrate the blood-brain barrier and be converted into ascorbic acid (AA) in the brain, exerting neuroprotective effects through its antioxidant action. Direct administration of AA, however, does not penetrate the blood-brain barrier and has no neuroprotective effect^[2].