BACKGROUND: The aim of the study was to find the cause of decreased activity of extracellular superoxide dismutase (EC SOD) in patients with diabetes-is it the decreased synthesis or increased glycation? METHODS: Total EC SOD activity, the activity of its fractions (A, B, and C) and its glycated form were determined in basal state and 30 min after intravenous (i.v.) administration of 50 mg of heparin. Patients were given i.v. heparin at a dose of 10,000 IU (100 mg) each 6 h for at least 3 days, and the activity of EC SOD was determined before the first heparin administration, just before each subsequent administration, and 30 min after heparin administration. RESULTS: Pre- and postheparinic activities of EC SOD and its fraction C in the group of patients with diabetes were significantly lower (p <0.001) than in control group. Preheparinic activities of EC SOD did not differ between the examined groups of patients. The postheparinic activities were different during the first 18 h of treatment. They were significantly lower in the group of patients with diabetes. During the following hours, after subsequently administered doses, there were no differences in the activity of EC SOD between the examined groups. Decline of EC SOD activity was observed after administration of repeated doses of heparin both in the examined and in the control groups. CONCLUSIONS: The decrease of extracellular superoxide dismutase activity in diabetes develops due to excessive glycation but not due to impaired synthesis. Therefore, appropriate glycemic control can lead to normalization of EC SOD activity.
BACKGROUND: The aim of the study was to find the cause of decreased activity of extracellular superoxide dismutase (EC SOD) in patients with diabetes-is it the decreased synthesis or increased glycation? METHODS: Total EC SOD activity, the activity of its fractions (A, B, and C) and its glycated form were determined in basal state and 30 min after intravenous (i.v.) administration of 50 mg of heparin. Patients were given i.v. heparin at a dose of 10,000 IU (100 mg) each 6 h for at least 3 days, and the activity of EC SOD was determined before the first heparin administration, just before each subsequent administration, and 30 min after heparin administration. RESULTS: Pre- and postheparinic activities of EC SOD and its fraction C in the group of patients with diabetes were significantly lower (p <0.001) than in control group. Preheparinic activities of EC SOD did not differ between the examined groups of patients. The postheparinic activities were different during the first 18 h of treatment. They were significantly lower in the group of patients with diabetes. During the following hours, after subsequently administered doses, there were no differences in the activity of EC SOD between the examined groups. Decline of EC SOD activity was observed after administration of repeated doses of heparin both in the examined and in the control groups. CONCLUSIONS: The decrease of extracellular superoxide dismutase activity in diabetes develops due to excessive glycation but not due to impaired synthesis. Therefore, appropriate glycemic control can lead to normalization of EC SOD activity.