ArticleAsian Pacific journal of cancer prevention : APJCP2017
Expression Changes of Apoptotic Genes in Tissues from Mice Exposed to Nicotine
Article in Asian Pacific journal of cancer prevention : APJCP, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Green-synthesized Desertifilum silver nanoparticles induce BAX/BCL-2 mediated apoptosis in Ehrlich carcinoma.BMC biotechnology · 2026Article
- Evaluating the anticancer efficacy of Chara vulgaris ethanolic extract and selenium nanoformulation in Ehrlich carcinoma mice: role of autophagy and apoptosis.BMC biotechnology · 2025Article
- Dexpanthenol protects against nicotine-induced kidney injury by reducing oxidative stress and apoptosis through activation of the AKT/Nrf2/HO-1 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Alpha7 Nicotinic Acetylcholine Receptor Mediates Nicotine-induced Apoptosis and Cell Cycle Arrest of Hepatocellular Carcinoma HepG2 Cells.Advanced pharmaceutical bulletin · 2020Article
- Effect of Harmine on Nicotine-Induced Kidney Dysfunction in Male Mice.International journal of preventive medicine · 2019Article
- The Effects of Thymoquinone Against Morphine-induced Damages on Male Mice Liver.International journal of preventive medicine · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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