Evaluation of DNA damage in tobacco associated human buccal cells using comet assay

Abstract

Aim and objective. To assess the DNA damage in tobacco associated human buccal cells using comet assay.
 Methods. The study included 75 study subjects, which were divided into 3 groups on the basis of tobacco usage. Group I - 25 individuals with no history of tobacco usage, Group II - 25 individuals with tobacco usage but without oral lesions and Group III - 25 individuals with tobacco associated oral lesions. Cytological smears collected from these individuals were used to assess the tobacco associated DNA damage by measuring the tail length in the comet assay method.
 Results. The average tail length was found to be 1.46 µm in the normal mucosa, 2.86 µm in tobacco users without oral lesions, 3.86 µm in the lesional sites of tobacco users and 3.67 µm in the non-lesional sites of these individuals. Factors like age, gender, duration and different forms of tobacco habit had their own impact on the oral mucosa.
 Conclusion. Comet assay helps assess the subclinical genetic changes of oral mucosa even before the clinical manifestations of the precancerous lesions appeared due to tobacco usage. Thus, comet assay may bloom out as a novel adjuvant tool for the prevention of oral cancer in the near future.

Evaluation of Cellular Changes and Immunohistochemistry Expression of p53 and p16 in the Oral Mucosa Among Saudi Smokers

“…It is also known as cyclin-dependent kinase inhibitor 2A (CDKN2A). The overexpression of P16 has been reported in several studies investigating oral cancer [ 7 ]. P53, on the other hand, is a tumor suppressor protein involved in regulating cell cycle progression and preventing the formation of tumors [ 8 ].…”

“…The association between smoking and the overexpression of P16 and p53 proteins in various tissues has been investigated in many studies. For example, Sunberg et al [7] found a significant increase in P16 expression among smokers compared to nonsmokers in oral squamous cell carcinoma. Similarly, Liu et al [11] reported a positive correlation between smoking and p53 overexpression in oral leukoplakia [12,13].…”