title: The involvement of peripheral polymorphonuclear leukocytes in the oxidative stress and inflammation among cigarette smokers.
abstract: BACKGROUND
  Cigarette smoking is a well-known risk factor for the development of endothelial dysfunction and the progression of atherosclerosis. Oxidative stress and inflammation have recently been implicated in endothelial dysfunction.
  
  
  OBJECTIVE
  To assess the concomitant contribution of polymorphonuclear leukocytes to systemic oxidative stress and inflammation in cigarette smokers.
  
  
  METHODS
  The study group comprised 41 chronic cigarette-smoking, otherwise healthy males aged 45.0 +/- 11.5 (range 31-67 years) and 41 male non-smokers aged 42.6 +/- 11.3 (range 31-65) who served as the control group. The potential generation of oxidative stress was assessed by measuring the rate of superoxide release from separated, phorbol 12-myristate 13-acetate-stimulated PMNL and by plasma levels of reduced (GSH) and oxidized (GSSG) glutathione. Inflammation was estimated indirectly by: a) determining the in vitro survival of PMNL, reflecting cell necrosis; b) in vivo peripheral PMNL counts, reflecting cell recruitment; and c) plasma alkaline phosphatase levels, indicating PMNL activation and degranulation.
  
  
  RESULTS
  PMA-stimulated PMNL from cigarette smokers released superoxide at a faster rate than PMNL from the controls. Smokers had decreased plasma GSH and elevated GSSG levels. In vitro incubation of control and smokers' PMNL in sera of smokers caused necrosis, while control sera improved smoker PMNL survival. Smokers' PMNL counts, although in the normal range, were significantly higher than those of controls. Plasma ALP levels in smokers were significantly higher than in controls and correlated positively with superoxide release and PMNL counts.
  
  
  CONCLUSIONS
  Our study shows that PMNL in smokers are primed in vivo, contribution concomitantly to systemic oxidative stress and inflammation that predispose smokers to endothelial dysfunction, and explains in part the accelerated atherosclerosis found in smokers.
authors.affiliation: Eliachar Research Laboratory, Nephrology and Hypertension Unit, Internal Department VI, Western Galilee Hospital, Nahariya, Israel.
authors.forename: Shifra
authors.initials: S
authors.lastname: Sela
authors.forename: Revital
authors.initials: R
authors.lastname: Shurtz-Swirski
authors.forename: Jamal
authors.initials: J
authors.lastname: Awad
authors.forename: Galina
authors.initials: G
authors.lastname: Shapiro
authors.forename: Lubna
authors.initials: L
authors.lastname: Nasser
authors.forename: Shaul M
authors.initials: SM
authors.lastname: Shasha
authors.forename: Batya
authors.initials: B
authors.lastname: Kristal
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D005978:Glutathione / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology*; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism*; D018384:Oxidative Stress; D012907:Smoking / Q000009:adverse effects*
chemical_list: D005978:Glutathione