BQ chewing contributes to the pathogenesis of cancer and oral cancer and OSF by T cell activation, induction of PGE2, tumor necrosis factor alpha (TNF-α) and IL-6 production, which affect oral mucosal inflammation and growth of oral fibroblast (OMF)

There are about 600 million people with the betel quid (BQ) chewing habit throughout the world (1). Studies showed that chewing BQ is associated with oral diseases, e.g. oral submucous fibrosis (OSF), oral leukoplakia (OL), and oral cancer (2-5). In addition, the alkaloid extracts from BQ have been characterized as carcinogenic (3-5), immunosuppressive, hepatotoxic (6), immunotoxic (7), genotoxic (8, 9), and teratogenic (9) materials. Also, arecoline, the major component in the BQ extracts, has been demonstrated to be mutagenic in mammalian cells (10, 11). Cyclooxygenase (COX) catalyzes the synthesis of PGs from arachidonic acid. COX-2 acts in the course of inflammatory processes and tissue repair and it is enhanced was by many of diverse stimuli including hormones, growth factors, cytokines, chemokines, environmental stress factors (12). A potential role of the COX-2 promoter region in the development of betelrelated oral cell carcinoma (OSCC) has been demonstrated. Prostaglandins exert their effects via prostanoid specific Gs coupled receptors (13). In 2003, Jeng et al. demonstrated that BQ chewing contributes to the pathogenesis of cancer and oral cancer and OSF by T cell activation, induction of PGE2, tumor necrosis factor alpha (TNF-α) and IL-6 production, which affect oral mucosal inflammation and growth of oral fibroblast (OMF) and oral epithelial cells (14). Chang et al. also have shown that U0126 and PD98059 (50 μM) decreased aerca nut (AN) extract and arecoline associated PGE2 and IL-6 production in GK and KB cells (11). Arecoline inhibits the secretion of cytokine seem via decrease the expression of COX-2 and PGE2 and then cytokine secret (11). JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY 2013, 64, 5, 535-543 www.jpp.krakow.pl