Fig. 1.

Tobacco smoke induces apoptosis and emphysematous lung damage in guinea pigs. (A) Representative histology from hematoxylin and eosin-stained lung sections of air exposed (sham controls) for 0 (i), 14 (ii), 21(iii), and 28 (iv) d against that of CS exposed for 0 (v), 14 (vi), 21 (vii), and 28 (viii) d, respectively, highlighting morphological changes in lung alveolar airspace (10 fields, n = 6). Alveolar morphometric changes depicted in A were expressed in terms of Lm (B) and Di (C) as indicators of lung damage. (D) Representative lung section profiles of the above treatment groups depicting alveolar cell apoptosis (green), as analyzed by (TUNEL) assay. Nuclei were stained with DAPI (blue) (10 fields, n = 6). (E) Immunoblots depicting time-dependent changes in lung elastin and MMP-9 levels with increasing CS exposure with corresponding change in pulmonary Bax (proapoptotic marker) and Bcl-2 (anti-apoptotic marker) expression levels. (F) Consequent increase in Bax/Bcl-2 expression ratio with time-dependent increase in CS exposure against sham controls shows virtually no change in levels of Bax or Bcl-2 (n = 6). Data were statistically analyzed by paired Student’s t test. Significant differences (*P < 0.05, **P < 0.01, ***P < 0.001) were observed in comparison with unexposed controls. Data are represented as means ± SD and are representative of three independent experiments done under similar conditions. (Scale bars: A, 50 µm; D, 100 µm.)