Generation of reactive oxygen species by a sufficient, insufficient and varicose vein wall

• Autorzy: Krzysciak W. , Kozka M.
• Języki publikacji: EN

Abstrakty

EN

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.

Słowa kluczowe

EN

chronic venous disease; leucocyte trapping; malonyldialdehyde; oxidative stress; reactive oxygen species; superoxide dismutase; varicose vein; vein wall; etiology; venous change; sufficient venous system; insufficient venous system

• Wydawca: -
• Czasopismo: Acta Biochimica Polonica
• Rocznik: 2011
• Tom: 58
• Numer: 1
• Opis fizyczny: p.89-94,fig.,ref.

Twórcy

autor

Krzysciak W.

• Department of Radioligand, Chair of Pharmacobiology, Faculty of Pharmacy, Jagiellonian University Medical College, Krakow, Poland

autor

Kozka M.

Bibliografia

• Benzie F, Iris F, Strain JJ (1996) The ferric reducing ability of plasma (FRAP) as a measure of "antioxidant power": the FRAP assay. Anal Biochem 239: 70-76. 
• Bergan J (2007) Molecular mechanisms in chronic venous insufficiency. Ann Vasc Surg 21: 260-266. 
• Bergan JJ, Pascarella L, Schmid-Schönbein GW (2008) Pathogenesis of primary chronic venous disease: Insights from animal models of venous hypertension. J Vasc Surg 47: 183-192. 
• Buege JA, Aust SD (1978) Microsomal lipid peroxidation. Methods Enzymol 52: 302-310. 
• Cooke M, Evans M, Dizdaroglu M (2003) Oxidative DNA damage: mechanism, mutation and disease. FASEB J 17: 1195-1214. 
• Cordis GA, Das DK, Riedel W (1998) High-performance liquid chromatographic peak identification of 2,4-dinitrophenylhydrazine derivatives of lipid peroxidation aldehydes by photodiode array detection. J Chromatogr A 798: 117--123. 
• Danielsson G, Norgren L, Truedsson L, Andreasson A, Danielsson P, Nilsson A, Swartbol P (2003) Flavonoid treatment in patients with heale venous ulcer: flow cytometry analysis suggests increased CD11b expression on neutrophil granulocytes in the circulation. Vasc Med 8: 83-88. 
• Drőge W (2002) Free radicals in the physiological control of cell function. Physiol Rev 82: 47-95. 
• Egyetem S, Orvostudomanyi A (2010) Chronic venous disease. A state of art. Orv Hetil. 151: 131-139. 
• Flore R, Santoliquido A, Antonio DL, Pola E, Flex A, Pola R, Gallinella Muzi M, Farinon A, Rulli F, Gaetani E et al. (2003) Long saphenous vein stripping reduces local level of reactive oxygen metabolites in patients with varicose disease of the lower limbs. World J Surg 27: 473-475. 
• Glowiński J, Glowiński S (2002) Generation of reactive oxygen metabolite by the varicose vein wall. Eur J Vasc Endovasc Surg 23: 550-555. 
• Halliwell B, Gutteridge JMC (2000) Free radicals in biology and medicine. 3rd edn. Oxford University Press. 
• Han L-N, Gu Y, Liu F-G (2005) Function of vasodilating and vasoconstricting factors in the pathogenesis of varicose vein. Chinese J Clin Rehab 9: 116-117.
• Heistad DD (2006) Oxidative stress and vascular disease: 2005 Duff Lecture. Arterioscler Thromb Vasc Biol 26: 689-695. 
• Jabłońska P, Krzyściak W et al. (2010) Oxidative stress in patients with CVD. Central European Congress Life Sciences, Krakow, Poland.
• James TJ, Hughes MA, Cherry GW, Taylor RP (2003) Evidence of oxidative stress in chronic venous ulcers. Wound Repair Regen 11: 172-176. 
• Kishimoto TK, Jutila MA, Berg EL, Butcher EC (1989) Neutrophil Mac-1 and MEL-14 adhesion proteins inversely regulated by chemotactic factors. Science 245: 1238-1241. 
• Krzyściak W et al. (2010) Oxidative DNA damage in blood of CVD patients taking Detralex. Central European Congress Life Sciences, Krakow, Poland.
• Madamanchi N, Vendrov A, Runge M (2005) Oxidative stress and vascular disease. Arterioscler Thromb Vasc Biol 25: 29-38. 
• Mangiafico RA, Malatino LS, Santonocito M, Spada RS, Benedetto FA (1997) Plasma endothelin-1 release in normal and varicose saphenous veins. Angiology 48: 769-774.  
• Matić M, Duran V, Ivkov-Simić M, Poljacki M, Gajinov Z, Begenisić M (2000) Microcirculatory changes in chronic venous insufficiency Med Pregl 53: 579-583.  
• Nicolaides A (2005) Chronic venous disease and leukocyte-endothelium interaction: from symptoms to ulceration. Angiology 56, Suppl 1: S11-S19. 
• Oliński R, Jurgowiak M (2002) Iron metabolizm, oxidative DNA damage and atherosclerosis. Acta Angiologia 8: 37-44.
• Peschen M, Lahaye T, Hennig B, Weyl A, Simon JC, Vanscheidt W (1999) Expression of the adhesion molecules ICAM-1, VCAM-1, LFA-1 and VLA-4 in the skin is modulated in progressing stages of chronic venous insufficiency. Acta Derm Venereol 79: 27-32. 
• R Development Team, R (2008) A Language and Environment for Statistical Computing. R Foundation for Statistical Computing; http://www.R.project.org. Graphs were produced with Statistica v. 7.0 PL.
• Rojas AI, Phillips TJ (1999) Patients with chronic leg ulcers show diminished levels of vitamins A and E, carotenes and zinc. Dermatol Surg 25: 601-604. 
• Slagsvold C, Stranden E, Rosales A (2009) Venous insufficiency in the lower limbs. Tidsskr Nor Laegeforen 129: 2256-2259. 
• Spitz DR, Oberley LW (1989) An assay for superoxide dismutase activity in mammalian tissue homogenates. Anal Biochem 179: 8-18. 
• Tryankina SA, Kolobova OI, Varshavsky BY (2003) Lipid peroxidation in pathogenesis of varix dilatation. Kliniczna Diagnostyka Laboratoryjna 6: 19-20 (in Polish).
• Valencia IC, Falabella A, Kirsner RS, Eaglstein WH (2001) Chronic venous insufficiency and venous leg ulceration. J Am Acad Dermatol 44: 401-421. 
• Wali MA, Suleiman SA, Kadoumi OF, Nasr MA (2002) Superoxide radical concentration and superoxide dismutase (SOD) enzyme activity in varicose vein. Ann Thorac Cardiovasc Surg 8: 286-290. 
• Wlaschek M, Scharffetter-Kochanek K (2005) Oxidative stress in chronic vein leg ulcers. Wound Repair Regen 13: 452-454. 
• Yasim A, Kilinc M, Aral M, Oksuz H, Kabalci M, Eroglu E, Imrek S (2008) Serum concentration of procoagulant, endothelial and oxidative stress markers in early primary varicose veins. Phlebology/Venous Forum of the Royal Society of Medicine. 23: 15-20. 
• Yeoh-Ellerton S, Stacey MC (2003) Iron and 8-isoprostane levels in acute and chronic wounds. J Invest Dermatol 121: 918-925.