Objectives The main question of this study was to evaluate the intensity of oxidative protein modification shown as advanced oxidation protein products (AOPP) and carbonylated proteins, expressed as protein carbonyl content (C=O) in abdominal aortic aneurysms (AAA), aortoiliac occlusive disease (AIOD), and chronic kidney disease (CKD). Design and Methods The study was carried out in a group of 35 AAA patients and 13 AIOD patients. However, CKD patients were divided into two groups: predialysis (PRE) included 50 patients or hemodialysis (HD) consisted of 34 patients. AOPP and C=O were measured using colorimetric assay kit, while C-reactive protein concentration was measured by high-sensitivity assay (hsCRP). Results The concentration of AOPP in both AAA and AIOD groups was higher than in PRE and HD groups according to descending order: AAA~AIOD > HD > PRE. The content of C=O was higher in the PRE group in comparison to AIOD and AAA according to the descending order: PRE~HD > AAA~AIOD. Conclusions AAA, AIOD, and CKD-related atherosclerosis (PRE and HD) contribute to the changes in the formation of AOPP and C=O. They may promote modification of proteins in a different way, probably due to the various factors that influence oxidative stress here.

SummaryBackgroundThe aim of this study was to evaluate serum iron concentration and influence of this element on biomarkers of oxidative stress in patients affected by chronic venous insufficiency (CVI).Material/MethodsSerum iron (SI) concentration and plasma parameters of oxidant–antioxidant balance (i.e., malonyldialdehyde [MDA], uric acid [UA] concentration, and total antioxidant capacity [TAC]) were compared between 35 patients divided into appropriate groups and 23 healthy individuals.ResultsThe subgroups analysis showed that SI concentration was significantly higher only in patients with shorter duration of CVI in comparison with the control group (P=0.013). Significant, negative correlation was found between SI concentration and duration of the disease (r=−0.422, P=0.014), age of the patients (r=−0.542, P=0.001) and BMI (r=−0.408, P=0.018). Mean value of MDA concentration and TAC capacity were higher in patients with CVI in comparison with healthy individuals (P<0.05). UA concentration was decreased, especially in CVI patients with mild clinical stage of disease and shorter CVI duration (P=0.047; P=0.034). There was no significant correlation found between SI concentration and the parameters of oxidant–antioxidant balance.ConclusionsHigh concentration of MDA and low UA level in blood of CVI patients suggests that oxidative stress plays an important role in the pathogenesis of the disease. The increase in SI concentration observed in the early stage of CVI can enhance free radicals formation; however, direct evidence has not been provided by the present study.

No abstract

STRESZCZENIEW pracy przedstawiono budowę witaminy C, jej właściwości fizyczne i chemiczne oraz występowanie. Wskazano na rolę biologiczną kwasu askorbinowego, zapotrzebowanie organizmu człowieka na tę witaminę i objawy jej niedoboru.

Background. The aim of the present study was to evaluate the concentration of serum thrombomodulin (sTM) in the AAA patients and to examine its correlation with various factors which may potentially participate in the endothelial injury. Materials and Methods. Forty-one patients with AAA were involved and divided into subgroups based on different criteria. Concentration of sTM was measured using enzyme-linked-immunosorbent assay (ELISA). The results were compared with those obtained in 30 healthy age- and sex-matched volunteers. Results. The higher concentration of sTM was observed in AAA patients compared with those in controls volunteers [2.37 (1.97–2.82) ng/mL versus 3.93 (2.43–9.20) ng/mL, P < 0.001]. An elevated sTM associated significantly with increased triglycerides (TAG) [P = 0.022], cholesterol [P = 0.029], hsCRP [P = 0.031], and advanced glycation end products (AGEs) [P = 0.033]. Conclusions. The elevation of serum sTM level suggests that endothelial damage occurs in AAA pathogenesis. The correlations observed indicate that lipids abnormalities, inflammation, and oxidative stress may be involved in this destructive process.