Abstract
The varicose vein results from the inefficient functioning of the valves in the lower limb veins, making the blood flow slow down and leading to blood stasis and hypoxia. This type of vein dysfunction might be a result of the development of oxidative stress. We compared oxidative stress markers in the plasma and erythrocytes obtained from peripheral veins and varicose veins in the same patients (glutathione, nonenzymatic antioxidant capacity (NEAC), catalase (CAT) and acetylcholinesterase (AChE) activity, thiols, thiobarbituric acid-reactive substance (TBARS), and protein carbonyls). We found a decrease in NEAC in the plasma obtained from the varicose veins compared to the peripheral veins. We detected a decrease in thiols in the plasma, hemolysate, and plasma membranes and increase in protein carbonyl compounds and TBARS levels in the varicose veins. These changes were accompanied by a decrease in CAT and AChE activity. For the first time, our results show changes in the plasma, erythrocyte membrane, and hemolysate protein properties in varicose vein blood in contrast to the plasma and erythrocytes in peripheral vein blood from the same patients. The increased oxidative stress accompanying varicose vein disease might result from the local inefficiency of the antioxidant defense system.
Highlights
For a long time, chronic venous disease (CVD) and its main clinical phenomenon—varicose veins (VV)—were often neglected and considered an aesthetic problem
We determined the properties of the plasma, erythrocyte membranes, and hemolysate obtained from varicose vein blood and normal peripheral vein blood in the same patients
To determine the total NEAC of the plasma, two independent methods were used. e changes in the NEAC measured with DPPH showed a significant decrease of NEAC in the plasma of a varicose vein in comparison to the plasma from a peripheral vein (p < .05) (Figure 2). e results obtained from the DPPH were similar to those observed using the ferric reducing ability of the plasma FRAP method (Figures 2(a) and 2(b))
Summary
Chronic venous disease (CVD) and its main clinical phenomenon—varicose veins (VV)—were often neglected and considered an aesthetic problem. E presence of varicose veins is the most common clinical symptom of chronic venous insufficiency or CVD affecting adult patients. Hormonal, and environmental factors trigger the development of venous system diseases, but age and pregnancy have been found to perform the most prominent role in developing varicose veins [1]. E hallmark of varicose veins is the insufficiency of the venous valves; the exact cause and molecular mechanisms leading to such a primary dysfunction have not yet been well identified [2]. Iron collection causes enhanced catalysis of free radical reactions that produce other reactive oxygen species (ROS) in the activated inflammatory cells present in venous blood, as well as those present in the wall of varicose veins. Iron collection causes enhanced catalysis of free radical reactions that produce other reactive oxygen species (ROS) in the activated inflammatory cells present in venous blood, as well as those present in the wall of varicose veins. is leads to the inflammation of the iron-controlled CVD of the lower limbs [3, 7]
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