L-arginine supplementation is hypothesized to reduce endothelial dysfunction and atherogenesis via increased biosynthesis of nitric oxide. Here we describe superoxide scavenging properties of arginine as an additional aspect which needs to be considered. Furthermore, arginine reduced copper-induced lipid peroxidation, indicating that superoxide anions essentially contribute to this process. In intact endothelial cells, L-arginine but not D-arginine diminished superoxide release and reduced cell-mediated breakdown of nitric oxide. Our data indicate that the reported vascular effects of L-arginine supplementation might involve an increased bioavailability of nitric oxide due to its superoxide scavenging properties beside a potential increased NO biosynthesis.