title: [Changes in oxidative stress and apoptosis parameters of neutrophils in rheumatoid diseases].
abstract: OBJECTIVE
  Study parameters of oxidative stress and apoptosis of neutrophils in patients with ankylosing spondylitis, systemic lupus erythematosus, systemic scleroderma and rheumatoid heart disease.
  
  
  METHODS
  240 patients with rheumatoid diseases and 25 healthy control group volunteers were examined. Neutrophil isolation from peripheral blood was performed by using double density gradient of ficoll-urografin. Cell functional activity was studied by chemiluminescence method. Pro-apoptosis antigen bak expression by neutrophils was studied by using streptavidin-biotin method. Griss reagent was used for nitrogen oxide production analysis.
  
  
  RESULTS
  An increase of oxygen dependent neutrophil metabolism processes was detected in patients with ankylosing spondylitis in comparison with systemic lupus erythematosus and systemic scleroderma patients. Systemic lupus erythematosus is characterized by higher biocidity of neutrophils in comparison with systemic scleroderma and rheumatoid heart disease. Increase of neutrophil granulocyte activity in ankylosing spondylitis is accompanied by an increase of superoxide-anion formation. In spite of high level of metabolic activity neutrophils in patients with ankylosing spondylitis have a low functional reserve, and neutrophils in patients with systemic scleroderma have the highest reserve potential.
  
  
  CONCLUSIONS
  Differences in expression parameters of oxidative stress by neutrophils depend on nosological form, varying by production level and active oxygen form formation reserve.
authors.forename: M V
authors.initials: MV
authors.lastname: Il'in
authors.forename: P A
authors.initials: PA
authors.lastname: Mal'tseva
authors.forename: D V
authors.initials: DV
authors.lastname: Rosanov
authors.forename: A S
authors.initials: AS
authors.lastname: Volkova
authors.forename: A O
authors.initials: AO
authors.lastname: Khrustalev
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000276:immunology; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D016022:Case-Control Studies; D003602:Cytotoxicity, Immunologic; D005260:Female; D006801:Humans; D049449:Luminescence; D008180:Lupus Erythematosus, Systemic / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis / Q000276:immunology; D018384:Oxidative Stress / Q000276:immunology; D017382:Reactive Oxygen Species / Q000276:immunology / Q000378:metabolism*; D012214:Rheumatic Heart Disease / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D012426:Russia; D012595:Scleroderma, Systemic / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D013167:Spondylitis, Ankylosing / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D050998:bcl-2 Homologous Antagonist-Killer Protein / Q000235:genetics / Q000378:metabolism
chemical_list: C494772:BAK1 protein, human; D017382:Reactive Oxygen Species; D050998:bcl-2 Homologous Antagonist-Killer Protein; D009569:Nitric Oxide