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Expression Changes of Apoptotic Genes in Tissues from Mice Exposed to Nicotine
Cyrus Jalili1, Mohammad Reza Salahshoor, Mohammad Taher Moradi
1Fertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Abstract:
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.
Insights
Nicotine exhibits dual apoptotic effects in mice: it is anti-apoptotic in the heart and lung but pro-apoptotic in the kidney and liver. These effects occur via a P53-independent pathway, influencing key apoptotic genes.
Area of Science:
- Toxicology
- Molecular Biology
- Pathology
Background:
- Smoking is a leading cause of preventable diseases, with nicotine being a key toxic component.
- The precise toxicity of nicotine, particularly its role in apoptosis, remains controversial.
- Understanding nicotine's cellular effects is crucial for public health and disease prevention.
Purpose of the Study:
- To investigate the apoptotic effects of nicotine on the heart, kidney, lung, and liver in male mice.
- To elucidate the molecular mechanisms underlying nicotine-induced apoptosis.
- To determine if nicotine's effects are mediated by the P53 pathway.
Main Methods:
- Male mice were treated with nicotine.
- Real-time PCR was used to quantify mRNA expression of apoptotic-related genes (P53, Bax, Caspase-2, Caspase-3).
- DNA fragmentation assays were performed on tissue samples from the heart, kidney, lung, and liver.
Main Results:
- Nicotine significantly decreased P53, Bax, and Caspase-3 mRNA expression in the heart and lung.
- Nicotine significantly increased Bax, Caspase-2, and Caspase-3 mRNA expression while decreasing P53 in the kidney and liver.
- DNA fragmentation was observed in the kidney and liver but not in the heart and lung of nicotine-treated mice.
Conclusions:
- Nicotine demonstrates anti-apoptotic effects on the heart and lung.
- Nicotine exhibits pro-apoptotic effects on the kidney and liver.
- These differential effects of nicotine on apoptosis occur through a P53-independent pathway.
