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Tobacco-related-compound-induced Nitrosative Stress Injury in the Hamster Cheek Pouch

Divisions of Oral & Maxillofacial Radiology and ¹ Oral & Maxillofacial Pathology, Department of Dentistry, Faculty of Medicine and Dentistry, University of Alberta, DPC 2085, Edmonton, AB T6G 2N8, Canada;

View larger version (36K): [in a new window]   Figure 1. Histopathologic changes in hamster cheek pouch epithelium following control, or tobacco-related-compound application. Mean incidence ± SD, and percentages (parentheses) are given. Scale bar represents 60 µm. Black arrow shows mitotic figure.

View larger version (26K): [in a new window]   Figure 2. Comet assay confirms DNA single-strand breaks induced by tobacco-related compounds. (A) Dose-dependent increase in comet tail moment with increasing smokeless tobacco extract. Each entity represents 1 POII cell. POII tail moment increases with increasing concentrations of smokeless tobacco extract (B), NNN and NNK (C), and nicotine (D). Each point is the mean ± standard error of 25 individual cells.

View larger version (60K): [in a new window]   Figure 3. 3-Nitrotyrosine immunoreactivity increases in hamster cheek pouch tissues with tobacco-related-compound application. (A) Tissue treated with DMSO/mineral oil; (B) smokeless tobacco extract; (C) nicotine; (D) NNN; and (E) NNK. Control epithelium shows 3-nitrotyrosine immunoreactivity confined to basal cells (arrows). All tobacco-related-compound treatments resulted in full-thickness 3-nitrotyrosine immunoreactivity. Scale bar represents 70 µm. (F) Mean gray level values ± SD of 3-nitrotyrosine intensity from 15 50 x 50 pixel regions of interest in 2 to 5 animals (* p < 0.005 compared with control).

View larger version (16K): [in a new window]   Figure 4. Biotransformation of nicotine to NNK via unstable intermediates (I,II), and aminoketone (after Hecht et al., 2000).