title: Secondhand Smoke Exposure Reduced the Compensatory Effects of IGF-I Growth Signaling in the Aging Rat Hearts.
abstract: 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.
authors.affiliation: 1. Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
authors.forename: Jia-Ping
authors.initials: JP
authors.lastname: Wu
authors.affiliation: 2. School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.
authors.forename: Dennis Jine-Yuan
authors.initials: DJ
authors.lastname: Hsieh
authors.affiliation: 3. Department of Biological Science and Technology, China Medical University, Taichung.
authors.forename: Wei-Wen
authors.initials: WW
authors.lastname: Kuo
authors.affiliation: 4. Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.
authors.forename: Chien-Kuo
authors.initials: CK
authors.lastname: Han
authors.affiliation: 5. Division of Cardiology, China Medical University Hospital, Taichung, Taiwan.
authors.forename: Peiying
authors.initials: P
authors.lastname: Pai
authors.affiliation: 6. Department of pathology, Changhua Christian Hospital, Changhua ; 7. Department of Medical Technology, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan.
authors.forename: Yu-Lan
authors.initials: YL
authors.lastname: Yeh
authors.affiliation: 8. Orthopaedic Department, Armed Forces General Hospital, Taichung, Taiwan.
authors.forename: Chien-Chung
authors.initials: CC
authors.lastname: Lin
authors.affiliation: 9. Department of Biotechnology, Bharathiar University, Coimbatore-641 046, India.
authors.forename: V Vijaya
authors.initials: VV
authors.lastname: Padma
authors.affiliation: 10. Department of Nursing, Mei Ho University, 23 Pingguang Road, Pingtung 91202, Taiwan.
authors.forename: Cecilia Hsuan
authors.initials: CH
authors.lastname: Day
authors.affiliation: 1. Graduate Institute of Basic Medical Science, China Medical University, Taichung, 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.
authors.forename: Chih-Yang
authors.initials: CY
authors.lastname: Huang
mesh_terms: D000375:Aging / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D053181:Caspase 8 / Q000378:metabolism; D053222:Fas Ligand Protein / Q000378:metabolism; D053200:Fas-Associated Death Domain Protein / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D007249:Inflammation / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D020257:Ventricular Remodeling / Q000187:drug effects; D019014:fas Receptor / Q000378:metabolism
chemical_list: C505535:Fadd protein, rat; D053222:Fas Ligand Protein; C491898:Fas protein, rat; D053200:Fas-Associated Death Domain Protein; C505662:Faslg protein, rat; D014028:Tobacco Smoke Pollution; D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor; D007334:Insulin-Like Growth Factor I; D051057:Proto-Oncogene Proteins c-akt; D053181:Caspase 8
keywords: Secondhand smoke exposure; age-related death-survival balance; aging; apoptosis.; cell cycle