Mitochondria are a rich source of O2• ̄, which is also supported by lethality of Mn-SOD deficiency [13,14], and mitochondrial O2• ̄ formation plays a central role for ischemia/reperfusion damage (e.g., during myocardial infarction (MI) and stroke) [65,66]. This evidence concerns the gene SOD2 and myocardial infarction.