Long-term hyperglycaemia decreases vascular fraction of extracellular superoxide dismutase

Excerpt

To the Editor: Diabetes mellitus is accompanied by more active processes of generating free oxygen radicals and simultaneously by a decreased rate of their removal. The intensity of these processes is proportional to the level of glycaemia and its duration. In diabetes, particularly when complicated by microangiopathy, a higher rate of oxidation of ascorbic acid, which is a non-specific scavenger of the superoxide radical was found [1]. The concentration of free radicals in body fluids of patients with diabetes could rise also as a result of changes in the activity of enzymes liberating oxygen radicals or a decrease in the activity of scavenging enzymes. A close inverse relationship between non-enzymatic glycation of proteins and the activity of superoxide dismutase in erythrocytes has been shown [2]. The only enzyme breaking down the superoxide radical in extracellular space is the extracellular superoxide dismutase (EC-SOD). Part of this enzyme is released into the bloodstream by fibroblasts and another is present on the surface of blood vessels. Administration of heparin into the bloodstream leads to the liberation of this fraction from the endothelium and its increased activity in plasma. Another study [3] has shown that glycation of EC-SOD decreases its affinity to heparin-Sepharose. Patients with diabetes have a higher percentage of glycated extracellular superoxide dismutase. Superoxide dismutase protects against an increase in the permeability of vessels caused by the superoxide radical and hypoxia. Reduced activity of the vascular fraction of EC-SOD could lead to higher levels of superoxide radical on the surface of endothelium and could activate the mechanism of diabetic microangiopathy. …