1. Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan
2. School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan
3. Department of Biological Science and Technology, China Medical University, Taichung
4. Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan
5. Division of Cardiology, China Medical University Hospital, Taichung, Taiwan
6. Department of pathology, Changhua Christian Hospital, Changhua
7. Department of Medical Technology, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan
8. Orthopaedic Department, Armed Forces General Hospital, Taichung, Taiwan
9. Department of Biotechnology, Bharathiar University, Coimbatore-641 046, India
10. Department of Nursing, Mei Ho University, 23 Pingguang Road, Pingtung 91202, Taiwan
11. School of Chinese Medicine, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan
12. Department of Health and Nutrition Biotechnology, Asia University, 500 Lioufeng Road, Taichung 41354, Taiwan
Background: Secondhand 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.
Methods: Rats 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.
Results: Death 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.
Conclusions: Aging reduces IGF-I compensated signaling with accelerated cardiac apoptotic effects from second-hand smoke.
Keywords: Secondhand smoke exposure, aging, age-related death-survival balance, cell cycle, apoptosis.