title: Ascorbate supplement reduces oxidative stress in dyslipidemic patients undergoing apheresis.
abstract: OBJECTIVE
  The effect of ascorbate treatment on apheresis-induced oxidative stress in uremic and dyslipidemic patients was evaluated.
  
  
  RESULTS
  We developed a chemiluminescence-emission spectrum and high-performance liquid chromatography analysis to assess the effect of ascorbate supplement on plasma reactive oxygen species (ROS) scavenging activity and oxidized lipid/protein production in hyperlipidemic and uremic patients undergoing apheresis. Apheresis was efficient in reduction of atherogenic lipoproteins, complement, fibrinogen, soluble intercellular adhesion molecule-1, and oxidative parameters including phosphatidylcholine hydroperoxide (PCOOH), malonaldehyde, methylguanidine, and diotyrosine. Apheresis itself, however, activated leukocytes to increase ROS activity and reduced the plasma ROS scavenging activity. Ascorbate administration selectively diminished apheresis-enhanced H2O2 and inflammatory mediators such as tumor necrosis factor alpha (TNF-alpha) and monocyte chemoattractant protein-1. Chronically dyslipidemic and uremic patients undergoing biweekly apheresis plus ascorbate treatment had lower levels of C-reactive protein and PCOOH than did those without ascorbate treatment during a 6-month follow-up study period.
  
  
  CONCLUSIONS
  We demonstrate that apheresis with ascorbate treatment provides a therapeutic potential in reducing atherosclerotic risk via inhibition of H2O2-induced oxidative stress in patients with uremia or dyslipidemia.
authors.affiliation: Department of Medical Research, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Chiang-Ting
authors.initials: CT
authors.lastname: Chien
authors.forename: Wei-Tien
authors.initials: WT
authors.lastname: Chang
authors.forename: Heui-Wen
authors.initials: HW
authors.lastname: Chen
authors.forename: Tzung-Dau
authors.initials: TD
authors.lastname: Wang
authors.forename: Shaw-Yih
authors.initials: SY
authors.lastname: Liou
authors.forename: Tzay-Jinn
authors.initials: TJ
authors.lastname: Chen
authors.forename: Yen-Lin
authors.initials: YL
authors.lastname: Chang
authors.forename: Yuan-Teh
authors.initials: YT
authors.lastname: Lee
authors.forename: Su-Ming
authors.initials: SM
authors.lastname: Hsu
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers; D002097:C-Reactive Protein / Q000032:analysis; D003131:Combined Modality Therapy; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000188:drug therapy / Q000378:metabolism / Q000628:therapy*; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D015227:Lipid Peroxidation; D008163:Luminescent Measurements; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008760:Methylguanidine / Q000097:blood; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010956:Plasmapheresis / Q000009:adverse effects*; D017382:Reactive Oxygen Species; D016897:Respiratory Burst; D016896:Treatment Outcome; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000097:blood; D014511:Uremia / Q000188:drug therapy / Q000378:metabolism / Q000628:therapy*; D014810:Vitamin E / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D000960:Hypolipidemic Agents; D017382:Reactive Oxygen Species; D014810:Vitamin E; D014443:Tyrosine; D008315:Malondialdehyde; D008760:Methylguanidine; D002097:C-Reactive Protein; C007543:dityrosine; D001205:Ascorbic Acid