Abstract
Vitamin B12 (B12) is required for cellular metabolism and DNA synthesis as a co-enzyme; it also possesses anti-reactive oxygen species (ROS) property as a superoxide scavenger. B12 deficiency has been implicated in multiple diseases such as megaloblastic anemia, and this disease can be effectively cured by supplementation of B12. Multiple studies suggest that B12 also benefits the conditions associated with excess ROS. Recently, we have reported that oral high dose B12 decreases superoxide level and renal injury induced by ischemia/reperfusion in mice. Here, we discuss potential mechanism(s) other than decreasing superoxide by which B12 executes its beneficial effects.
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