Tobacco Smoking and Liver Cancer Risk: Potential Avenues for Carcinogenesis
Citation
Divya Jain,1 Priya Chaudhary,1 Nidhi Varshney,1 Khandaker Sabit Bin Razzak,2 Devret Verma,3 Tasnim Reza Khan Zahra,4 Pracheta Janmeda,1 Javad Sharifi-Rad , 5 Sevgi Durna Das¸tan,6,7 Shafi Mahmud,8 Anca Oana Docea,9 and Daniela Calina 10 1 Department of Bioscience and Biotechnology, University of Banasthali Vidyapith, Rajasthan, India 2 Department of Public Health, American International University, Dhaka, Bangladesh 3 Department of Biotechnology, Graphic Era (Deemed to Be University), Dehradun- 248 002 Uttarakhand, India 4 Department of Genetic Engineering and Biotechnology, East West University, Dhaka, Bangladesh 5 Facultad de Medicina, Universidad del Azuay, Cuenca, Ecuador 6 Department of Biology, Faculty of Science, Sivas Cumhuriyet University, 58140 Sivas, Turkey 7 Beekeeping Development Application and Research Center, Sivas Cumhuriyet University, 58140 Sivas, Turkey 8 Genetic Engineering and Biotechnology, University of Rajshahi, Rajshahi, Bangladesh 9 Department of Toxicology, University of Medicine and Pharmacy of Craiova, Craiova, Romania 10Department of Clinical Pharmacy, University of Medicine and Pharmacy of Craiova, Craiova, RomaniaAbstract
Smoking a cigarette generates over 4000 chemicals that have a deleterious impact on each part of the human body. It produces
three main severe effects on the liver organ: oncogenic, immunological, and indirect or direct toxic effects. It results in the
production of cytotoxic substances, which raises fibrosis and necro-inflammation. Additionally, it also directs the production of
pro-inflammatory cytokines tumour necrosis factor alfa (TNF-α) and interleukins (IL-1β, IL-6) that will be responsible for the
chronic liver injury. Furthermore, it gives rise to secondary polycythemia and successively raises the turnover and mass of red
cells, which might be a common factor responsible for the development of oxidative stress in the liver due to iron overload. It also
produces chemicals that are having oncogenic properties and raises the risk of liver cancer especially in sufferers of chronic
hepatitis C. Smoking modulates both humoral and cell-mediated responses by restricting the proliferation of lymphocytes and
inducing their apoptosis and ultimately decreasing the surveillance of cancer cells. Moreover, it has been determined that heavy
smoking impacts the response of hepatitis C patients to interferon (IFN) therapy through different mechanisms, which can be
improved by phlebotomy. Efforts are being made in different nations in decreasing the prevalence of smoking to improve
premature death and ill effects of their nation’s individuals.
