138 Dental Journal (Majalah Kedokteran Gigi) 2019 September; 52(3): 138–141 Research Report Effects of sidestream tobacco smoke on P53 expressions in Rattus novergicus tongue epithelial mucosa Dian Angriany, 1 Diah Savitri Ernawati, 1 Adiastuti Endah Parmadiati, 1 Hening Tuti Hendarti 1 and Rosnah Binti Zain 2 1 Department of Oral Medicine, Faculty of Dental Medicine, Universitas Airlangga, Surabaya – Indonesia 2 Department of Oral Pathology and Oral Medicine, Faculty of Dentistry, MAHSA University, Bandar Saujana Putra – Malaysia ABSTRACT Background: Smoking, both active and passive, has been widely recognised as toxic to the human body, since it induces several forms of cancer, including that affecting the oral cavity. Benzopyrene, the carcinogen contained in tobacco smoke, can even lead to carcinogenesis which potentially affects the regulation of cell apoptosis in both active and passive smokers. Purpose: This study aims to investigate the carcinogenic effects of cigarette smoke on apoptosis of rat tongue mucosae through p53 expression. To determine the risk of malignant transformation through tumor suppressor genes in the apoptotic pathway. Methods: Rattus norvegicus subjects were divided into four groups, namely Treatment Group 1 exposed to sidestream cigarette smoke for four weeks (P1), Treatment Group 2 exposed to sidestream cigarette smoke for eight weeks (P2), Control Group not exposed to sidestream cigarette smoke for four weeks (K2), and Control Group (K) not exposed to sidestream cigarette smoke for eight weeks (K2). The exposure process was conducted using a smoking pump and alternating exposure. Four micron-thick sections of formalin were subsequently fixed together with paraffin embedded biopsy material from tongue mucosa of Rattus norvegicus. The tissue sections from the treatment groups were then analyzed immunohistochemically to compare the expressions of p53 and Bcl-2 proteins with those of the control groups. Results: The T-test results indicated statistically significant differences in the expressions of p53 between the 4-week control group (K1) and the 4-week treatment group (P1) (p=0.01, p<0.05) as well as between the 8-week control group (K2) and the 8-week treatment group (P2) (p=0.03, p<0.05). Conclusion: Exposure to cigarette smoke can induce changes in tumor suppressor genes and also affect the regulation of cell apoptosis, thus changing cell structure and leading to malignancy. Keywords: apoptosis; carcinogenesis; sidestream cigarette smoke; p53; tongue mucosa Correspondence: Diah Savitri Ernawati, Department of Oral Medicine, Faculty of Dental Medicine, Universitas Airlangga. Jl. Mayjend. Prof. Dr. Moestopo no. 47 Surabaya 60132, Indonesia. E-mail: diah-s-e@fkg.unair.ac.id INTRODUCTION Over the last 50 years, numerous studies have been conducted on the toxic chemicals contained in cigarette smoke which are regarded as carcinogens for humans. Cigarette smoke is one risk factor for oral cancer in both active and passive smokers due to the presence of carcinogenic elements that can potentially induce cancer. Passive smokers inhale the second-hand environmental cigarette smoke exhaled by active smokers. Smoke inhaled by passive smokers can also cause health problems similar to those experienced by active smokers since it contains approximately 200 toxic substances, 69 of which are carcinogenic. These carcinogens form covalent bonds with DNA (DNA adducts) subsequently inducing carcinogenesis. 1,2 The correlation between both active and passive smoking and carcinogenesis has actually been studied and identified to exist in several forms of cancer. A high risk of smoking-related cancers also relates to the head and neck. These include cancer of the oral cavity, pharynx and larynx, in addition to lung cancer. 3 The process of carcinogenesis is a somatic event thought to be caused by accumulative genetic and epigenetic changes affecting the normal molecular control settings in cell proliferation. These genetic changes can subsequently deactivate the tumor suppressor gene, thereby triggering tumor formation. 4 The tumor suppressor gene (p53 gene) is a transcription factor that activates a large number of Dental Journal (Majalah Kedokteran Gigi) p-ISSN: 1978-3728; e-ISSN: 2442-9740. Accredited No. 32a/E/KPT/2017. Open access under CC-BY-SA license. Available at http://e-journal.unair.ac.id/index.php/MKG DOI: 10.20473/j.djmkg.v52.i3.p138–141