The present study is the first report to prove that VC depletion results in an increase of superoxide generation. In the living
Adriamycin modeled here, ischemia-reperfusion of brain slices from VC-depleted SMP30/GNL KO mice showed that the latter’s superoxide levels were significantly higher than those of matched controls with a normal VC content and of their WT counterparts. In vitro, VC is known to scavenge superoxide generated by the xanthine-xanthine oxidase system [2], singlet oxygen generated photochemically by using ultraviolet light and hematoporphyrin as a sensitizer [3], and hydroxyl radicals generated by exposure to ionizing radiation [4]. Measuring the ROS accurately in living tissues and whole animals is very difficult, because ROS is highly reactive and has an extremely short life span. Therefore, little direct evidence exists to verify that VC actually scavenges ROS in a physiologic setting. Here, we overcame this problem by using a real-time biographic system [19] in which Lucigenin is a chemiluminescence probe that detects superoxide anion radicals. Lucigenin represent superoxide production within
cells and tissues at physiological pH [20] and [21].
