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Hemodialysis (HD) patients are characterized by impaired T-cell function at least in part because of T-cell zeta-chain downregulation due to inflammation. Angiogenin responds as an acute phase reactant, is increased in HD patients, suppresses T-cell function and increased angiogenin level is co-localized with T-cell zeta-chain downregulation in various pathologies. Angiogenin can inhibit translation of proteins, which lack internal ribosomal entry sites in the corresponding mRNAs. In this study, the possible effect of angiogenin on T-cell zeta-chain downregulation was evaluated. Thirty HD patients and 21 healthy volunteers participated. T-cell zeta-chain expression was assessed with flow cytometry, plasma angiogenin and serum IL-6 with ELISA and serum C-reactive protein with an immunoturbidimetric method. Two available software tools were used for predicting the presence or not of internal ribosomal entry sites in T-cell zeta-chain mRNA sequence. In silico analysis of T-cell zeta-chain mRNA sequence failed to reveal the presence of internal ribosomal entry sites. T-cell zeta-chain expression was lower in HD patients than in healthy volunteers (1.86 ± 0.63 vs. 4.73 ± 3.22). In HD patients, C-reactive protein as well as IL-6 were higher than in healthy volunteers (10.04 ± 15.13 mg/L vs. 3.43 ± 0.98 mg/L and 15.06 ± 13.08 pg/mL vs. 2.11 ± 2.10 pg/mL respectively). Angiogenin was higher in HD patients than in healthy volunteers (483.20 ± 154.07 ng/mL vs. 259.98 ± 64.15 ng/mL). Neither C-reactive protein, nor IL-6 was associated with angiogenin or T-cell zeta-chain expression. Angiogenin concentration was negatively related to the expression of T-cell zeta-chain (r = -0.410, P = 0.025). Increased angiogenin may contribute to decreased T-cell zeta-chain expression in HD patients., (© 2012 The Authors. Therapeutic Apheresis and Dialysis © 2012 International Society for Apheresis.)

Oxidative stress is increased in hemodialysis (HD) patients and contributes to the increased morbidity and mortality in this population. Vitamin E is an antioxidant agent. In the present study the effect of prolonged oral alpha-tocopherol administration on the antioxidant defense system was evaluated. The antioxidant factors plasma total antioxidant status (TAS), red blood cell superoxide dismutase (SOD) activity and glutathione peroxidase (GPX) activity were evaluated with spectrometry in 27 HD patients. Measurements were performed before and after oral administration of alpha-tocopherol at a dose of 500 mg/d for a one-year period. Twenty HD patients received a placebo and 22 healthy volunteers served as controls. TAS was increased in HD patients. No difference was detected in SOD and GPX activity between HD patients and healthy volunteers. Tocopherol administration induced a significant decrease in TAS and SOD activity. Levels of GPX activity remained unaffected. All the evaluated factors remained stable in the HD patients receiving a placebo. Prolonged oral alpha-tocopherol administration in HD patients induces a decrease in some components of the antioxidant defense system, raising the possibility for a pro-oxidative role of vitamin E. Vitamin E is an antioxidant agent, but it is also known to have pro-oxidant action under special conditions that can be encountered in HD patients.