title: No acute impact of haemodialysis treatment on free radical scavenging enzyme gene expression in white blood cells.
abstract: OBJECTIVE
  Oxidative stress has been implicated in the side-effects caused by haemodialysis (HD) treatment.
  
  
  METHODS
  In the present study we have investigated whether gene expression of the enzymatic defence system provided by cellular glutathione peroxidase (GPx-1), phospholipid glutathione peroxidase (GPx-4), glutathione reductase (GSSG-R), glutathione synthethase (GSH-S), Cu/Zn-superoxide dismutase (SOD-1) and catalase (CAT) is affected by HD. The GPx-1, GPx-4, GSSG-R, GSH-S, SOD-1 and CAT mRNA were determined in white blood cells by quantitative reverse transcriptase-polymerase chain reaction with the LightCycler instrument and transcription elongation factor-2 as reference gene at the start (SD) and immediately after (ED) dialysis treatment (n = 36). In a subgroup (n = 10), messenger RNA (mRNA) expression was determined hourly during a 5 h HD.
  
  
  RESULTS
  The expression of GPx-1, GPx-4, GSSG-R, GSH-S, SOD-1 and CAT mRNA was not affected by a single HD treatment. All mRNAs were significantly (P < 0.05) increased in HD patients [median (16. percentiles (perc.); 84. perc.)]: GPx-1: 2.18 (0.89; 3.23); GPx-4: 0.41 (0.26; 0.74); GSSG-R: 0.04 (0.02; 0.10); GSH-S: 0.04 (0.02; 0.08); SOD-1: 0.32 (0.20; 0.62); CAT: 0.12 (0.06; 0.18) when compared with healthy blood donors (GPx-1: 0.91 (0.60; 1.44); GPx-4: 0.27 (0.16; 0.43); GSSG-R: 0.02 (0.01; 0.02); GSH-S: 0.02 (0.02; 0.04); SOD-1: 0.15 (0.10; 0.18); CAT: 0.07 (0.04; 0.16).
  
  
  CONCLUSIONS
  These results show that the HD procedure does not acutely affect the antioxidant defence system on the gene level but suggest that the chronic stress caused by uraemia and/or HD may cause gene induction of the enzymatic defence system.
authors.affiliation: Department of Nephrology and Rheumatology, Division of Internal Medicine, Georg-August-University, Robert-Koch-Strasse 40, Göttingen, Germany. vschett@gwdg.de
authors.forename: V
authors.initials: V
authors.lastname: Schettler
authors.forename: W
authors.initials: W
authors.lastname: Kühn
authors.forename: T
authors.initials: T
authors.lastname: Kleinoeder
authors.forename: V W
authors.initials: VW
authors.lastname: Armstrong
authors.forename: M
authors.initials: M
authors.lastname: Oellerich
authors.forename: G A
authors.initials: GA
authors.lastname: Müller
authors.forename: E
authors.initials: E
authors.lastname: Wieland
mesh_terms: D000368:Aged; D005260:Female; D005609:Free Radicals / Q000378:metabolism*; D015870:Gene Expression; D006801:Humans; D007962:Leukocytes / Q000201:enzymology*; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D010088:Oxidoreductases / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D006435:Renal Dialysis; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013482:Superoxide Dismutase / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D000099156:Superoxide Dismutase 2
chemical_list: D005609:Free Radicals; D010088:Oxidoreductases; D012333:RNA, Messenger; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D000099156:Superoxide Dismutase 2; C000606290:SOD1 protein, human