title: Impaired synthesis is not the reason for decreased activity of extracellular superoxide dismutase in patients with diabetes.
abstract: 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.
authors.affiliation: Department of Nephrology, Transplantology and Internal Medicine, Pomeranian Medical University, Szczecin, Poland. kazcie@sci.pam.szczecin.pl
authors.forename: Kazimierz
authors.initials: K
authors.lastname: Ciechanowski
authors.forename: Karolina
authors.initials: K
authors.lastname: Kedzierska
authors.forename: Edyta
authors.initials: E
authors.lastname: Gołembiewska
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Safranow
authors.forename: Joanna
authors.initials: J
authors.lastname: Bober
authors.forename: Leszek
authors.initials: L
authors.lastname: Domański
authors.forename: Jacek
authors.initials: J
authors.lastname: Rózański
authors.forename: Marek
authors.initials: M
authors.lastname: Myślak
mesh_terms: D000328:Adult; D000368:Aged; D003922:Diabetes Mellitus, Type 1 / Q000201:enzymology*; D003924:Diabetes Mellitus, Type 2 / Q000201:enzymology*; D005109:Extracellular Matrix; D005260:Female; D005947:Glucose / Q000378:metabolism; D006442:Glycated Hemoglobin / Q000032:analysis; D006493:Heparin / Q000008:administration & dosage; D006801:Humans; D008297:Male; D008875:Middle Aged; D013482:Superoxide Dismutase / Q000097:blood*
chemical_list: D005947:Glucose; D006442:Glycated Hemoglobin; D006493:Heparin; D013482:Superoxide Dismutase