Insulin Release from the Beta Cells in Acatalasemic Mice Is Highly Susceptible to Alloxan-Induced Oxidative Stress

Background: Catalase deficiency (acatalasemia) is sensitive to alloxan, and the administration to acatalasemic mice develops hyperglycemia under mild conditions. However, the mechanism is still poorly understood. Methods: Alloxan was used to induce the oxidative stress and intraperitoneal-ly administered to acatalasemic and normal mice. The blood samples of these mice after 1, 3, 5 and 7 days were examined. The pancreatic islets 7 days after alloxan administration were isolated, and the insulin released under 3 mM and 20 mM glucose was examined. Results: After alloxan admin-istration, increase of oxidative markers in blood and pancreatic apoptosis in acatalasemic mice were observed immediately. Insulin in blood was lowered after 3 days, and the insulin in acatala-semic mice was lower than that in normal mice. Hyperglycemia in the acatalasemic mice was ob-served after 3 days. The pancreatic islets after 7 days were isolated. A reduction of the insulin re