BACKGROUND AND AIMS: Patients with chronic renal failure, especially those treated with haemodialysis, have an increased risk of developing atherosclerotic vascular disease probably as a result of enhanced oxidative stress. The human cell membrane possesses electron transfer systems which protect against extracellular pro-oxidant challenge. We evaluated (1) the erythrocyte velocity of ferricyanide reduction (RBC vfcy) in 25 uraemic patients (aged 25-71 years; 14 males), (2) the changes induced by a single haemodialysis session and (3) biomarkers of oxidative stress. METHODS AND RESULTS: Before and after a mid-week dialysis session, we measured RBC vfcy, erythrocyte glutathione (RBC GSH), plasma and red cell membrane malondialdehyde (P and RBC MDA), plasma sulphydryl groups (P SH), plasma vitamin C levels and haemolysis percentage. Pre-dialysis RBC GSH (0.68+/-0.13 vs 0.80+/-0.13 mg/mL, p<0.01), P SH (266+/-74 vs 406+/-78 micromol/L, p<0.01) and plasma vitamin C (7.0+/-5.1 vs 21.5+/-8.5mg/L, p<0.001) were lower than in 25 age-sex-matched healthy controls; P MDA (1.57+/-0.52 vs 0.54+/-0.29 nmol/mL, p<0.001), RBC MDA (0.42+/-0.13 vs 0.34+/-0.16 nmol/mL, p<0.05) and haemolysis (1.2+/-0.3 vs 0.7+/-0.3%, p<0.001) were increased. Baseline RBC vfcy did not differ from normals (13.1+/-5.2 vs 12.9+/-3.2 mmol/mL/h). Following dialysis, RBC vfcy (to 8.9+/-4.5 mmol/mL/h, p<0.001) decreased, as well as P MDA, RBC MDA and plasma vitamin C (to 2.5+/-1.4 mg/L, p<0.001), whereas P SH groups increased (to 413+/-99 micromol/L, p<0.001); haemolysis percentage remained high. RBC vfcy values were correlated to RBC GSH and vitamin C levels. CONCLUSIONS: Uraemic patients showed signs of oxidative stress. Pre-dialysis RBC vfcy is maintained in the normal range on account of a reduced intracellular content of GSH and in spite of low plasma ascorbate. A single haemodialysis treatment reduced biomarkers of protein and lipid oxidation but markedly impaired transmembrane electron transfer, which could be explained by acute depletion of electron donors.
BACKGROUND AND AIMS: Patients with chronic renal failure, especially those treated with haemodialysis, have an increased risk of developing atherosclerotic vascular disease probably as a result of enhanced oxidative stress. The human cell membrane possesses electron transfer systems which protect against extracellular pro-oxidant challenge. We evaluated (1) the erythrocyte velocity of ferricyanide reduction (RBC vfcy) in 25 uraemic patients (aged 25-71 years; 14 males), (2) the changes induced by a single haemodialysis session and (3) biomarkers of oxidative stress. METHODS AND RESULTS: Before and after a mid-week dialysis session, we measured RBC vfcy, erythrocyte glutathione (RBC GSH), plasma and red cell membrane malondialdehyde (P and RBC MDA), plasma sulphydryl groups (P SH), plasma vitamin C levels and haemolysis percentage. Pre-dialysis RBC GSH (0.68+/-0.13 vs 0.80+/-0.13 mg/mL, p<0.01), P SH (266+/-74 vs 406+/-78 micromol/L, p<0.01) and plasma vitamin C (7.0+/-5.1 vs 21.5+/-8.5mg/L, p<0.001) were lower than in 25 age-sex-matched healthy controls; P MDA (1.57+/-0.52 vs 0.54+/-0.29 nmol/mL, p<0.001), RBC MDA (0.42+/-0.13 vs 0.34+/-0.16 nmol/mL, p<0.05) and haemolysis (1.2+/-0.3 vs 0.7+/-0.3%, p<0.001) were increased. Baseline RBC vfcy did not differ from normals (13.1+/-5.2 vs 12.9+/-3.2 mmol/mL/h). Following dialysis, RBC vfcy (to 8.9+/-4.5 mmol/mL/h, p<0.001) decreased, as well as P MDA, RBC MDA and plasma vitamin C (to 2.5+/-1.4 mg/L, p<0.001), whereas P SH groups increased (to 413+/-99 micromol/L, p<0.001); haemolysis percentage remained high. RBC vfcy values were correlated to RBC GSH and vitamin C levels. CONCLUSIONS: Uraemic patients showed signs of oxidative stress. Pre-dialysis RBC vfcy is maintained in the normal range on account of a reduced intracellular content of GSH and in spite of low plasma ascorbate. A single haemodialysis treatment reduced biomarkers of protein and lipid oxidation but markedly impaired transmembrane electron transfer, which could be explained by acute depletion of electron donors.