TY - JOUR ID - 43070 TI - Expression Changes of Apoptotic Genes in Tissues from Mice Exposed to Nicotine JO - Asian Pacific Journal of Cancer Prevention JA - APJCP LA - en SN - 1513-7368 AU - Jalili, Cyrus AU - Salahshoor, Mohammad Reza AU - Moradi, Mohammad Taher AU - Ahookhash, Maryam AU - Taghadosi, Mehdi AU - Sohrabi, Maryam AD - Fertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran. AD - Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran. AD - Students Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran. AD - Department of Immunology, Kermanshah University of Medical Sciences, Kermanshah, Iran. Y1 - 2017 PY - 2017 VL - 18 IS - 1 SP - 239 EP - 244 KW - Nicotine KW - Apoptosis KW - Liver KW - Caspase-2 KW - p53 DO - 10.22034/APJCP.2017.18.1.239 N2 -   Objective: Smoking is the leading preventable cause of various diseases such as lung cancer, chronic obstructive pulmonary disease and cardiovascular disease. Nicotine, one of the major toxic components of tobacco, contributes to the pathogenesis of different diseases. Methods: Given the controversy about nicotine toxicity, the present study was conducted to determine apoptotic effects of nicotine on the heart, kidney, lung and liver of male mice. Real-time PCR was performed to identify mRNA expression changes in apoptotic-related genes between nicotine treated and control mice. Result: In the heart and lung, nicotine caused significant decrease in P53, Bax and Caspase-3 mRNA expression levels compared to the control group. However, in the kidney and liver, the result was significant increase in Bax, Caspase-2, Caspase-3 and a significant decrease in P53 mRNA expression (p<0.01). DNA fragmentation assays indicated no fragmentation in the heart and lung, but in the kidney and liver of nicotine treated mice, isolated DNA was fragmented. Conclusion: Our study provided insight into the molecular mechanisms of nicotine anti-apoptotic effects on the heart and lung as well as pro-apoptotic effects on kidney and liver via a P53-independent pathway. UR - https://journal.waocp.org/article_43070.html L1 - https://journal.waocp.org/article_43070_e070b9a96096b48b6bb42993b7fbc898.pdf ER -