The glucose-derived cellular damage has been related to a hyperglycemia-induced overproduction of mitochondrial reactive oxygen species (ROS), resulting in defective ROS homeostasis and in the inactivation of antioxidant responses, in particular superoxide dismutase-2 (SOD-2) and glutathione peroxidase-1 (GPx-1), which are responsible for controlling the rate of radicals produced under stress conditions. This evidence concerns the gene SOD2 and Hyperglycemia.