• Jia-Ping Wu, Dennis Jine-Yuan Hsieh, Wei-Wen Kuo, Chien-Kuo Han, Peiying Pai, Yu-Lan Yeh, Chien-Chung Lin, V Vijaya Padma, Cecilia Hsuan Day, and Chih-Yang Huang.
• 1. Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
• Int J Med Sci. 2015 Jan 1; 12 (9): 708-18.

BackgroundSecondhand smoke (SHS) exposure is associated with increased risk of cardiovascular disease. Aging is a physiological process that involves progressive impairment of normal heart functions due to increased vulnerability to damage. This study examines secondhand smoke exposure in aging rats to determine the age-related death-survival balance.MethodsRats were placed into a SHS exposure chamber and exposed to smog. Old age male Sprague-Dawley rats were exposed to 10 cigarettes for 30 min, day and night, continuing for one week. After 4 weeks the rats underwent morphological and functional studies. Left ventricular sections were stained with hematoxylin-eosin for histopathological examination. TUNEL detected apoptosis cells and protein expression related death and survival pathway were analyzed using western blot.ResultsDeath receptor-dependent apoptosis upregulation pathways and the mitochondria apoptosis proteins were apparent in young SHS exposure and old age rats. These biological markers were enhanced in aging SHS-exposed rats. The survival pathway was found to exhibit compensation only in young SHS-exposed rats, but not in the aging rats. Further decrease in the activity of this pathway was observed in aging SHS-exposed rats. TUNEL apoptotic positive cells were increased in young SHS-exposed rats, and in aging rats with or without SHS-exposure.ConclusionsAging reduces IGF-I compensated signaling with accelerated cardiac apoptotic effects from second-hand smoke.

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