The present study showed consistent results in the increased levels of oxidative stress products and its related DNA damage markers (e.g., 8-OHdG and γ-H2AX), and in the lower activity of antioxidant enzyme (e.g., SOD), supporting the increase of oxidative stress in metabolic syndrome and its component pathologies [6, 7, 12, 22, 23]. This evidence concerns the gene SOD1 and metabolic syndrome.