Inhibition of tobacco smoke-induced lung inflammation by a catalytic antioxidant

Kevin R. Smith, Dale L. Uyeminami, Urmila P. Kodavanti, James D. Crapo, Ling Yi Chang, Kent E Pinkerton

Research output: Contribution to journalArticlepeer-review

112 Scopus citations


Cigarette smokers experience airway inflammation and epithelial damage, the mechanisms of which are unknown. One potential cause may be free radicals either in tobacco smoke or produced during persistent inflammation. Inflammation may also be a driving force to cause airway epithelium to undergo changes leading to squamous cell metaplasia. To test whether tobacco smoke-induced inflammation could be reduced by a catalytic antioxidant, manganese(III)meso-tetrakis(N,N′-diethyl-1,3-imidazolium-2-yl) porphyrin (AEOL 10150) was given by intratracheal instillation to rats exposed to filtered air or tobacco smoke. Exposure to tobacco smoke for 2 d or 8 weeks (6 h/d, 3 d/week) significantly increased the number of cells recovered by bronchoalveolar lavage (BAL). AEOL 10150 significantly decreased BAL cell number in tobacco smoke-treated rats. Significant reductions in neutrophils were noted at 2 d and macrophages at 8 weeks. Lymphocytes were significantly reduced by AEOL 10150 at both time points. Squamous cell metaplasia following 8 weeks of tobacco smoke exposure was 12% of the total airway epithelial area in animals exposed to tobacco smoke without AEOL 10150, compared with 2% in animals exposed to tobacco smoke, but treated with AEOL 10150 (p < .05). We conclude that a synthetic catalytic antioxidant decreased the adverse effects of exposure to tobacco smoke.

Original languageEnglish (US)
Pages (from-to)1106-1114
Number of pages9
JournalFree Radical Biology and Medicine
Issue number8
StatePublished - Oct 15 2002


  • AEOL 10150
  • Catalytic antioxidant
  • Free radicals
  • Inflammation
  • Metalloporphyrins
  • Squamous cell metaplasia
  • Tobacco smoke

ASJC Scopus subject areas

  • Medicine(all)
  • Toxicology
  • Clinical Biochemistry


Dive into the research topics of 'Inhibition of tobacco smoke-induced lung inflammation by a catalytic antioxidant'. Together they form a unique fingerprint.

Cite this