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INHIBITION OF TOBACCO SMOKE-INDUCED LUNG INFLAMMATION BY A CATALYTIC ANTIOXIDANT
Citation:
Smith, K., D. L. Uyeminami, U P. Kodavanti, J. D. Crapo, L. Y. Chang, AND K. E. Pinkerton. INHIBITION OF TOBACCO SMOKE-INDUCED LUNG INFLAMMATION BY A CATALYTIC ANTIOXIDANT. Free Radical Biology and Medicine. Elsevier Science BV, Amsterdam, Netherlands, 33(8):1106-1114, (2002).
Description:
AMathematical Model for the Kinetics of the Male Reproductive Endocrine System
Laura K. Potter1,2, H.A. Barton2 and R.W. Setzer2
1Curriculum in Toxicology, UNC-Chapel Hill, NC; 2US EPA, ORD, NHEERL, ETD, RTP, NC
In this presentation a model for the hormonal regulation of the reproductive endocrine system in the adult male rat will be discussed. The model includes a description of the kinetics of the androgenic hormones testosterone and dihydrotestosterone, as well as the receptor-mediated regulation of prostate size and function by these two androgens. Numerical and parameter estimation methods for the resulting system of differential algebraic equations will be presented. (This abstract does not reflect EPA policy.)
Kevin R. Smith, Dale L Uyeminami, Urmila P. Kodavanti, James D. Crapo, Ling-Yi Chang, and Kent E. Pinkerton. INHIBITION OF TOBACCO SMOKE-INDUCED LUNG INFLAMMATION BY A CATALYTIC ANTIOXIDANT.
Cigarette smokers experience inflammation and epithelial damage of their airways. However, the mechanisms for this inflammation and injury are not well established. One potential cause may be the formation of free radicals leading to oxidative stress. It has been estimated that as high as 1016 free radicals are present per puff of tobacco smoke. Persistent airway inflammation may also be a driving force to cause the epithelium to undergo changes leading to mucous and squamous cell metaplasia. To test whether tobacco smoke-induced inflammation could be reduced by a catalytic antioxidant, AEOL 10150 was given by intratracheal instillation to spontaneously hypertensive rats exposed to filtered air or tobacco smoke. Tobacco smoke concentration was 80 mg/m3 particulates, 3.6 mg/m3 nicotine, and 275 ppm CO. Exposure was for 2 days or 8 weeks (6 hours/day, 3 days/week). Exposure to tobacco smoke significantly increased the number of cells recovered by bronchoalveolar lavage (BAL). Instillation of AEOL 10150 significantly decreased BAL cell number in tobacco smoke-treated rats. Significant reductions in neutrophils were noted at 2 days and alveolar macrophages at 8 weeks. Lymphocytes were also significantly reduced following AEOL 10150 instillation at 2 days and 8 weeks. Squamous cell metaplasia following 8 weeks of tobacco smoke exposure was 12% of the total airway surface 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<0.05). We conclude AEOL 10150 can attenuate in part the adverse effects of exposure to tobacco smoke.