Immunoperoxidase detection of polycyclic aromatic hydrocarbon-DNA adducts in mouth floor and buccal mucosa cells of smokers and nonsmokers

A. Besarati Nia, H.W.M. van Straaten, R.W.L. Godschalk, N. van Zandwijk, A.J.M. Balm, J.C.S. Kleinjans, F.J. van Schooten*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Tobacco smoking is a major risk Factor For oral cancer; mouth floor and buccal mucosa are among the most and least cancer-prone subsites, respectively, in the oral cavity. We investigated the applicability of immunohisiochemistry of smoking-induced DNA adducts in oral cells for assessing the exposure to carcinogens, and estimating the risk for oral cancer. Polycyclic aromatic hydrocarbon (PAH)-DNA adducts were measured in mouth Floor and buccal mucosa cells of smokers (n = 26) and nonsmokers (n = 22) by means of a semiquantitative immunoperoxidase assay. Smokers had elevated levels of PAH-DNA adducts compared to nonsmokers in their mouth floor cells (0.045 +/- 0.022 versus 0.022 +/- 0.016, P = 0.0008 arbitrary units of immunohistochemistry) as well as in their buccal mucosa cells (0.058 +/- 0.028 versus 0.028 +/- 0.012, P = 0.001). Also, there was a correlation between the levels of PAH-DNA ad-ducts in mouth floor cells and those in buccal mucosa cells (r = 0.4, P = 0.01). Furthermore, PAH-DNA adduct levels in both mouth floor and buccal mucosa cells were significantly related to current smoking indices (amount of tar and number of cigarettes consumed per day). Expectedly, the levels of PAH-DNA adducts neither in mouth floor cells nor in buccal mucosa cells, both being short-lived cells, were related to smoking history index (pack years). The levels of PAH-DNA adducts, however, in mouth floor cells as the cancer prone cells were lower than those in buccal mucosa cells (0.037 +/- 0.023 versus 0.044 +/- 0.026, P = 0.04). We conclude that immunohistochemistry of PAH-DNA adducts in oral cells can be used For exposure assessment of tobacco-related carcinogens, however, it cannot be used for oral cancer risk estimation.
Original languageEnglish
Pages (from-to)127-133
Number of pages7
JournalEnvironmental and Molecular Mutagenesis
Volume36
DOIs
Publication statusPublished - 1 Jan 2000

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