Erythrocyte transmembrane electron transfer in haemodialysis patients.
OBJECTIVE
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.


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.
Matteucci
Elena
E
Department of Internal Medicine, University of Pisa, Via Rome 67, 56126 Pisa, Italy. ematteuc@int.med.unipi.it
Cupisti
Adamasco
A
Caprioli
Raffaele
R
Battipaglia
Elena
E
Favilla
Stefania
S
Rindi
Paolo
P
Barsotti
Giuliano
G
Giampietro
Ottavio
O
D000328:Adult; D000368:Aged; D001205:Ascorbic Acid / Q000378:metabolism; D004579:Electron Transport; D004910:Erythrocyte Membrane / Q000378:metabolism*; D005260:Female; D005609:Free Radicals; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D006435:Renal Dialysis; D013438:Sulfhydryl Compounds / Q000097:blood
D005609:Free Radicals; D013438:Sulfhydryl Compounds; D008315:Malondialdehyde; D001205:Ascorbic Acid