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Am J Physiol Lung Cell Mol Physiol 290: L396-L404, 2006. First published October 7, 2005; doi:10.1152/ajplung.00483.2004
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Tomato juice prevents senescence-accelerated mouse P1 strain from developing emphysema induced by chronic exposure to tobacco smoke

Satoshi Kasagi,1 Kuniaki Seyama,1 Hiroaki Mori,1 Sanae Souma,1 Tadashi Sato,1 Taeko Akiyoshi,1 Hiroyuki Suganuma,2 and Yoshinosuke Fukuchi1

1Department of Respiratory Medicine, Juntendo University School of Medicine, Tokyo; and 2Kagome Research Institute, Kagome, Nasu-gun, Tochigi, Japan

Submitted 29 December 2004 ; accepted in final form 24 September 2005

The senescence-accelerated mouse (SAM) is a naturally occurring animal model for accelerated aging after normal development and maturation. SAMP1 strain was reported to show age-related structural and functional changes in lung and to be a murine model of senile lung. We postulated that aging of lung is an important intrinsic process for development of emphysema and even in a short period of tobacco smoke exposure may be able to generate emphysema. At age 12 wk, SAMP1 inhaled air or 1.5% tobacco smoke (total particulate matter 23.9 mg/m3) through the nose for 30 min/day, 5 days/wk, and for 8 wk. The mean linear intercepts (MLI) and destructive index (DI) of lung were significantly increased [air vs. smoke (means ± SE); MLI, 68.76 ± 0.69 vs. 75.34 ± 1.70 µm, P < 0.05 and DI, 8.61 ± 0.38 vs. 16.18 ± 1.54%, P < 0.05], whereas no significant changes were observed in SAMR1, control mice that show normal aging. In contrast, smoke-induced emphysema was completely prevented by concomitant ingestion of lycopene given as tomato juice [MLI: smoke with/without lycopene (mean ± SE), 62.87 ± 0.8 vs. 66.90 ± 1.33 µm, P < 0.05]. Smoke exposure increased apoptosis and active caspase-3 of airway and alveolar septal cells and reduced VEGF in lung tissues, but tomato juice ingestion significantly reduced apoptosis and increased tissue VEGF level. We conclude that SAMP1 is a useful model for tobacco smoke-induced emphysema and a valuable tool to explore both pathophysiological mechanisms and the effect of therapeutic intervention on smoke-induced emphysema.

oxidant; antioxidant; vascular endothelial growth factor; apoptosis; aging



Address for reprint requests and other correspondence: K. Seyama, Dept. of Respiratory Medicine, Juntendo Univ., School of Medicine, 2-1-1 Hongo, Bunkyo-Ku, Tokyo 113-8421, Japan (e-mail: kseyama{at}med.juntendo.ac.jp)




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