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ATTENUATED EXPRESSIONS OF SOD‐1 IN THE MESENTERIC ARTERIAL TISSUE OF STREPTOZOTOCIN (STZ)‐INDUCED DIABETIC RATS

Various studies have found that oxidative stress, which can be due to an increase in the production of reactive oxygen species (ROS) and/or a decrease in the elimination of ROS by enzymatic antioxidants, plays a critical role in vascular dysfunction that is associated with diabetic mellitus. Our study performed Western blot analysis of superoxide dismutase (SOD), endothelial nitric oxide synthase (eNOS), and inducible nitric oxide synthase (iNOS) of mesenteric arterial (MA) tissues of control, 6‐ and 12‐week STZ‐induced diabetic Sprague‐Dawley rats with blood glucose levels of 113 ± 4.24, 598 ± 4.47, and > 600 mg/dl, respectively. Our results showed an increase in eNOS (>1 fold), iNOS (>4 fold), and SOD (>8 fold) expressions in the 6‐wk STZ MA tissues (n=5) versus control tissues (n=5). The results also showed relatively unchanged levels of eNOS, increased iNOS (>1 fold), and increased SOD (>5 fold) expressions in 12‐wk STZ MA tissues (n=3) versus control tissues. Past studies have shown an increase in the production of ROS at 6 weeks of STZ diabetes, which is sustained through 12 weeks of the disease in the rat aortic tissue. Our study suggests that diabetes initially stimulates a compensatory increase in SOD expression, which attenuates as the disease progresses to 12 weeks. Supported by grant #T35‐HL071486 from the NIH.