title: Gender difference in systemic oxidative stress and antioxidant capacity in current and former heavy smokers.
abstract: BACKGROUND
  Several studies suggested that women may be more susceptible to oxidative damage induced by cigarette smoking, but the role of smoking status and antioxidant capacity in gender difference in susceptibility to oxidative damage has not been well studied.
  
  
  METHODS
  We conducted a cross-sectional analysis of the baseline data from 146 current and former heavy smokers enrolled in a chemoprevention trial to determine the gender difference in oxidative damage and antioxidant capacity. Oxidative DNA and lipid damage were assessed by urinary 8-hydroxy-2'-deoxyguanosine (8OHdG) and 8-isoprostaglandin F(2α) (8-iso-PGF(2α)), respectively. The erythrocyte antioxidant enzymes and serum fat-soluble antioxidants were measured to assess antioxidant capacity.
  
  
  RESULTS
  Female smokers had significantly greater levels of 8OHdG and 8-iso-PGF(2α) than males but the gender difference was only significant in current smokers. No gender difference was noted in erythrocyte antioxidant enzymes, although female current smokers had significantly lower or a trend for lower antioxidant enzymes. Female smokers had higher serum β-carotene than males. Biomarkers of oxidative damage did not correlate significantly with the antioxidant enzymes. Urinary 8OHdG did not correlate significantly with fat-soluble antioxidants. Inverse correlations were observed between urinary 8-iso-PGF(2α) and several serum carotenoids.
  
  
  CONCLUSIONS
  Female current smokers have a greater extent of oxidative damage despite having higher serum levels of fat-soluble antioxidants. Lower erythrocyte antioxidant enzymes in female current smokers may contribute to the greater extent of oxidative damage.
  
  
  CONCLUSIONS
  The study may help identify appropriate high-risk populations for interventions that attenuate oxidative damage and appropriate biomarkers for clinical studies in smokers.
authors.affiliation: The University of Arizona Cancer Center, Tucson, AZ, USA.
authors.forename: Iman A
authors.initials: IA
authors.lastname: Hakim
authors.forename: Robin
authors.initials: R
authors.lastname: Harris
authors.forename: Linda
authors.initials: L
authors.lastname: Garland
authors.forename: Catherine A
authors.initials: CA
authors.lastname: Cordova
authors.forename: Dalia M
authors.initials: DM
authors.lastname: Mikhael
authors.forename: H-H
authors.initials: HH
authors.lastname: Sherry Chow
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000975:Antioxidants / Q000378:metabolism*; D003430:Cross-Sectional Studies; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D004912:Erythrocytes / Q000201:enzymology / Q000378:metabolism; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D018570:Risk Assessment; D012307:Risk Factors; D012737:Sex Factors; D012907:Smoking / Q000097:blood / Q000235:genetics / Q000378:metabolism* / Q000652:urine
chemical_list: D000975:Antioxidants; C075750:8-epi-prostaglandin F2alpha; D000080242:8-Hydroxy-2'-Deoxyguanosine; D015237:Dinoprost; D003849:Deoxyguanosine