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 be a murine model of senile lung. We postulated that aging of lung is an important intrinsic process for the development of emphysema and even in a short period of tobacco-smoke exposure may be able to generate emphysema. At age of 12 weeks, SAMP1 inhaled air or 1.5% tobacco smoke (TPM 23.9 mg/m³) through the nose for 30 min per day, 5 days per week, and for 8 weeks. The mean liner intercepts (MLI) and destructive index (DI) of the lung were significantly increased (air vs. smoke (mean±SEM); 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 observed in SAMR1, control mice that shows normal aging. In contrast, smoke-induced emphysema was completely prevented by concomitant ingestion of lycopene (a potent antioxidant) given as tomato juice, (MLI: smoke with or without lycopene (mean±SEM), 62.87±0.8 vs. 66.90±1.33µm, 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 concluded that SAMP1 is a useful model for tobacco-smoke induced emphysema and a valuable tool to explore both pathophysiologic mechanisms and the effect of therapeutic intervention on smoke-induced emphysema.