title: Increased DNA damage in patients with chronic obstructive pulmonary disease who had once smoked or been exposed to biomass.
abstract: OBJECTIVE
  Chronic obstructive pulmonary disease (COPD) is a slowly progressive condition characterised by poorly reversible airflow limitation associated with an abnormal inflammatory response of the lung. The main causal factors of COPD are chronic oxidative stress as a result of long-term smoking, use of biomass fuels, and air pollution. In this study, basal levels of DNA strand breaks were investigated together with some additional oxidative markers implicating oxidative damage on the other biomolecules such as proteins and lipids in patients with COPD who were exposed to smoking and biomass.
  
  
  METHODS
  We detected DNA strand breaks in peripheral blood mononuclear leukocytes by using a Single Cell Gel Electrophoresis (also called Comet Assay), plasma protein carbonyl (PC) content by using Reznick and Parker's spectrophotometric method, and lipid peroxidation by measurement of malondialdehyde (MDA) as indexes of oxidative stress in 47 patients with smoking-related COPD and 25 patients with biomass-related COPD and 36 age-and-sex matched control participants.
  
  
  RESULTS
  The mean values of DNA strand breaks, MDA and protein carbonyl levels were significantly higher in smoking- and biomass-related COPD groups than in the control group (ANOVA P<0.001, <0.05 and <0.05, respectively). DNA damage levels were also higher in smoking-related COPD group than in biomass-related COPD group (P<0.05). There was a positive relationship between DNA damage and MDA levels in smoking-related COPD group (P<0.05).
  
  
  CONCLUSIONS
  Oxidative stress markers and DNA damage were strongly increased in both patient groups with smoking- and biomass-related COPD. However, DNA is more affected in smoking-related COPD patients than in biomass-related COPD. These data indicate that cigarette smoking is a more significant DNA damaging risk factor than biomass smoke.
authors.affiliation: Department of Chest Disease, Medical Faculty, Harran University, Sanliurfa, Turkey. drerkanceylan@yahoo.com
authors.forename: Erkan
authors.initials: E
authors.lastname: Ceylan
authors.forename: Abdurrahim
authors.initials: A
authors.lastname: Kocyigit
authors.forename: Mehmet
authors.initials: M
authors.lastname: Gencer
authors.forename: Nurten
authors.initials: N
authors.lastname: Aksoy
authors.forename: Sahbettin
authors.initials: S
authors.lastname: Selek
mesh_terms: D000368:Aged; D000393:Air Pollutants / Q000009:adverse effects; D016902:Air Pollution, Indoor / Q000009:adverse effects*; D018533:Biomass; D003296:Cooking; D004249:DNA Damage; D004736:Energy-Generating Resources; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D018384:Oxidative Stress; D050050:Protein Carbonylation; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000209:etiology / Q000235:genetics*; D012906:Smoke / Q000009:adverse effects; D012907:Smoking / Q000009:adverse effects / Q000097:blood / Q000235:genetics*; D014797:Vital Capacity
chemical_list: D000393:Air Pollutants; D012906:Smoke; D008315:Malondialdehyde