Antioxidative mechanism in the course of varicose veins

Abstract

Objective Our objective was to evaluate the state of oxidative stress in the great saphenous varicose vein wall and blood of varicose vein patients taken from the antecubital vein. Methods The superoxide dismutase, reduced glutathione (GSH) and total antioxidant status were measured with commercially available colorimetric kits in erythrocytes, plasma and varicose vein wall of 65 patients (second degree of clinical state classification, etiology, anatomy and pathophysiology) aged 22-70 (49 women, 16 men) in comparison to normal great saphenous vein walls collected from 10 patients who underwent coronary artery bypass graft and blood collected from 20 healthy individuals. Results A statistically significant decrease (p < 0.001) in superoxide dismutase activity in erythrocytes and the increase (p < 0.05) in superoxide dismutase activity in varicose vein has been observed. There have been no significant changes in the concentration of GSH in plasma and in varicose vein. The decreased concentration of total antioxidant status in plasma (p < 0.001) and in varicose vein wall (p < 0.05) in comparison to the control has been noticed. Conclusion The varicose vein patients are affected by oxidative stress. Our results indicate impaired antioxidant defense mechanism in the blood of varicose vein patients. In contrast to the blood, an increased process of antioxidant defense in the varicose vein wall was noticed.

Effects of the oxidative stress and genetic changes in varicose vein patients

“…Research findings studying the Gpx and GST, and thus GSH levels in tissue homogenates of VVs and their association with the disease are controversial. 6,26,31,32 In our study, CAT levels were found to be higher than the control group. In the context of the study, MDA and CAT levels were found to be higher than control group and SOD, GPx and GST levels were found to be lower than the control group.…”

“…Research findings studying the Gpx and GST, and thus GSH levels in tissue homogenates of VVs and their association with the disease are controversial. 6,26,31,32…”

“…Every triggered biochemical process results in the production of another exacerbating process in a cycle and suggested to have a role in the pathogenesis of VVs. 6,7 Hemochromatosis gene (HFE) C282Y gene variant was shown to be associated with VV in different population types, suggesting that the increased levels of free iron can be inducing the generation of free radicals by the Fenton reaction, and initiates and/or exacarbates endothelial cell dysfunction. 8,9 Malondialdehyde (MDA) is formed as a result of the conversion of lipid hydroperoxides to aldehydes and carbonyl compounds thus being an indirect indicator of the level of oxidative damage in the systemic circulation and an important marker used to determine the level of the ROS in the organism.…”

“…Every triggered biochemical process results in the production of another exacerbating process in a cycle and suggested to have a role in the pathogenesis of VVs. 6,7…”

Alterations in the Plasma and Red Blood Cell Properties in Patients with Varicose Vein: A Pilot Study

“…e main destructive factor is venous hypertension, which may lead to the remodeling of vein walls and vein valves due to an increase in venous pressure, which leads to structural and functional changes in the vein wall. Various studies have hypothesized that the cause of CVD is the trapping of leukocytes owing to the defective valves and oxidative stress in the veins [3][4][5]. In addition, hypoxia performs a significant role in the physiopathology of varicose veins [6].…”