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Despite numerous theories, the etiology and pathogenesis of primary varicose veins remain unclear. The etiology of chronic venous diseases (CVDs) known as chronic venous insufficiency (CVI) is related to leukocyte trapping. Leukocyte trapping involves trapping of white cells in vessel walls followed by their activation and translocation outside the vessel. Release of reactive oxygen species (ROS) from trapped white cells has been documented. Superoxide dismutase (SOD) directly inhibits the generation of free radicals and compounds that are produced during oxidation by ROS, such as malonyldialdehyde (MDA). The aim of this study was to determine the involvement of free radicals in the etiology of venous changes. The following material was used for the study: fragments of sufficient or insufficient venous system and varices from 31 patients diagnosed with chronic venous disease in the 2nd or 3rd degree, according to clinical state, etiology, anatomy and pathophysiology (CEAP), which were qualified for surgical procedure. The levels of oxidative stress markers strongly correlated with lesions observed by USG in insufficient and varicose veins. In both a higher concentration of MDA was observed, which is a sign of lipid peroxidation. Antioxidative mechanisms, SOD activity and total antioxidative power expressed as FRAP were inversely proportional to MDA concentration. In insufficient and varicose veins both FRAP and SOD activities were significantly lower than in normal veins. The severity of clinical changes was inversely dependent on the efficiency of scavenging of ROS, which additionally proves the participation of free radicals in pathogenesis of CVDs.
Severe burn injury is associated with damage of tissues and organs distant to the area of injury. Although different agents are suggested to play an important role in pathogenesis of the burn disease, disturbed balance between the development of reactive oxygen forms and activity of antioxidants can play a pivotal role. Therefore, the aim of our study was to examine the intensity of lipid peroxidation process in plasma and lung tissues as well as the antioxidant ability of rats subjected to severe burn injury during 48 hrs after the injury. Our results show that severe burn injury causes a significant increase in the level of lipid peroxides in plasma and lung tissues, with a concomitant increase in superoxide dismutase (Cu-Zn SOD) activity in erythrocytes during 48 hrs of the postburn period. Glutathione peroxidase (Se-GPx) activity in whole blood was significantly higher during the first postburn day and then decreased becoming lower than that found in the healthy subjects. Total Antioxidant Status (TAS) and the level of uric acid in plasma also increased. Thus, we conclude that severe burn injury causes the imbalance between the intensity of the lipid peroxidation process and the antioxidant ability of the organism and this can play an important role in the pathophysiology of the burn disease.
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