title: Vitamin C reversed malfunction of peripheral blood-derived mononuclear cells in smokers through antioxidant properties.
abstract: BACKGROUND
  Smoking impairs neovascularization, possibly, through the impaired function of peripheral blood-derived mononuclear cells (PB-MNCs). Thus, the mechanism of impaired function of PB-MNCs caused by chronic smoking was examined, and whether vitamin C reversed the malfunction of PB-MNCs in smokers was investigated.
  
  
  RESULTS
  The cohort comprised 27 healthy male volunteers (16 smokers and 11 age-matched non-smokers). For evaluation of the colony-forming activity of PB-MNCs, the number of endothelial colony-forming units (e-CFUs) was counted in a culture assay. Migration activity of PB-MNCs was evaluated by the modified Boyden chamber method. In smokers, the number of e-CFUs was reduced to 56% and migratory activity of PB-MNCs to 40% compared with non-smokers (p<0.01). The urinary level of 8-isoprostane, an oxidative stress marker, was greater in smokers than in non-smokers (p<0.05). There was an inverse correlation between migratory activity of PB-MNCs but not between the number of e-CFUs and urinary level of 8-isoprostane. Furthermore, oral administration of vitamin C for 2 weeks ameliorated the impaired migratory activity of PB-MNCs in smokers.
  
  
  CONCLUSIONS
  Chronic smoking impairs the function of PB-MNCs. Smoking-induced oxidative stress may be involved in impaired migratory activity of PB-MNCs.
authors: Division of Cardiovascular Medicine, Department of Medicine, Kurume University School of Medicine, Kurume, Japan.
authors: Yoshiaki
authors: Y
authors: Takeshita
authors: Yoshio
authors: Y
authors: Katsuki
authors: Yousuke
authors: Y
authors: Katsuda
authors: Hisashi
authors: H
authors: Kai
authors: Yutaka
authors: Y
authors: Saito
authors: Ken
authors: K
authors: Arima
authors: Ken-Ichiro
authors: K
authors: Sasaki
authors: Tsutomu
authors: T
authors: Imaizumi
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D016022:Case-Control Studies; D002465:Cell Movement / Q000187:drug effects; D015331:Cohort Studies; D003114:Colony-Forming Units Assay; D016207:Cytokines / Q000097:blood; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D042783:Endothelial Cells / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D008297:Male; D018384:Oxidative Stress; D012907:Smoking / Q000097:blood* / Q000188:drug therapy* / Q000473:pathology / Q000652:urine; D042461:Vascular Endothelial Growth Factor A / Q000097:blood / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D016207:Cytokines; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D001205:Ascorbic Acid