[Evaluation of oxidative stress parameters in diabetes 2 patients in different stage of metabolic compensation]

Etiopathogenesis of vascular complications in diabetes is complex and multifactorial. One of the factors that is connected both with chronic complications of diabetes and intensification of oxidative stress is long-term hyperglicaemia. It has been noted that control improvement of glicaemia delays and/or inhibits the development of further complications. The aim of the study was to evaluate selected parameters of oxidative stress in patients with metabolic compensated or decompensated diabetes by means of marking in red blood cells of the patients in question the activity of antioaxidative enzymes such as: superoxide dysmutase (SOD-1) and catalase (CAT) and concentration of malondialdehyde (MDA). 61 diabetic patients took part in the research, 31 of which met the criteria of metabolic compensation whereas 30 were metabolically decompensated. The reference group (K) consisted of 40 healthy men. The activity of SOD-1 was marked by Misra and Fridovich's method, the activity of CAT by Beers and Sizer's method and the concentration of MDA in red blood cells was indicated by Placer et al. The activity of evaluated antioxidative enzymes SOD-1 and CAT in the erythrocytes of diabetes type 2 patients was statistically lower as compared with the control group. The highest activity of SOD-1 and CAT was noted in metabolic decompensated diabetes type 2 group. The concentration of MDA in diabetes type 2 patients red blood cells was significantly higher as compared with the control group. Significantly higher concentration of MDA was noted in metabolically decompensated diabetic patients comparing to patients with proper metabolically compensated diabetes. The obtained results confirm the toxicity of glucose. Long-term hyperglicaemia through activation of different metabolic paths leads to the intensification of free radical processes and attenuation of antioxidative mechanisms.