title: Oxidative stress during dialysis: effect on free radical scavenging enzyme (FRSE) activities and glutathione (GSH) concentration in granulocytes.
abstract: BACKGROUND
  Living cells are protected by free radical scavenging enzymes against oxygen radical-mediated damage. It has been suggested that granulocytes are activated on the surface of dialyser membranes, resulting in the generation of free radicals. We have recently reported a lack of plasma lipid peroxidation and unchanged glutathione peroxidase (GSH-Px) as well as glutathione reductase (GSSG-R) activities in red blood cells of haemodialysis patients. However, because mature red cells are free of DNA and RNA, free radical scavenging enzymes (FRSE) cannot be regulated on the gene level in response to an acute oxidative stress. In contrast to erythrocytes, granulocytes are nucleated cells and FRSE protein concentrations can therefore be modulated.
  
  
  METHODS
  GSH-Px, GSSG-R, superoxide dismutase (SOD) activities and total glutathione (GSH) were determined spectrophotometrically using a Cobas Fara semi-automatic analyser in granulocytes of 31 healthy blood donors and in 28 patients with chronic renal failure (CRF) for more than 6 months before as well as immediately after a single dialysis treatment. Patients were treated either by haemodialysis (n = 17) using low-flux polysulphone membranes or by haemofiltration (n= 1l) usings high-flux polysulphone membranes.
  
  
  RESULTS
  Compared to healthy controls, SOD and GSSG-R activities were increased in granulocytes of HD and HF patients, GSH and GSH-Px were decreased before a single treatment. After dialysis SOD and GSH-PX activities were significantly induced by both HD and HF whereas GSSG-R activities and GSH were decreased.
  
  
  CONCLUSIONS
  These results show that the enzymatic defence against oxygen radicals can be induced in granulocytes of patients undergoing regular dialysis treatment, whereas the non-enzymatic defence is compromised as shown by decreased GSH concentrations, both suggesting increased oxidative stress.
authors.affiliation: Department of Nephrology and Rheumatology, Georg-August-University, Göttingen, FRG.
authors.forename: V
authors.initials: V
authors.lastname: Schettler
authors.forename: E
authors.initials: E
authors.lastname: Wieland
authors.forename: H
authors.initials: H
authors.lastname: Methe
authors.forename: P
authors.initials: P
authors.lastname: Schuff-Werner
authors.forename: G A
authors.initials: GA
authors.lastname: Müller
mesh_terms: D000328:Adult; D000368:Aged; D005260:Female; D005500:Follow-Up Studies; D016166:Free Radical Scavengers / Q000097:blood; D005978:Glutathione / Q000097:blood*; D005979:Glutathione Peroxidase / Q000097:blood; D005980:Glutathione Reductase / Q000097:blood; D006098:Granulocytes / Q000201:enzymology*; D017583:Hemodiafiltration; D006801:Humans; D007676:Kidney Failure, Chronic / Q000201:enzymology* / Q000628:therapy; D008297:Male; D018384:Oxidative Stress; D010088:Oxidoreductases / Q000097:blood*; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: D016166:Free Radical Scavengers; D010088:Oxidoreductases; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione