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Abstract
Betel quid (BQ)-chewing is a popular oral habit with potential links to the occurrence
of oral cancer. Many of the literature-based studies reveal that areca nut (AN) extract
may demonstrate mutagenic and genotoxic effects, in addition to inducing preneoplastic
as well as neoplastic lesions in experimental animals. Areca nut should, thus, be
highly suspected as a human carcinogen. Toxicity studies relating to AN-contained
polyphenols and tannins are not conclusive, with both carcinogenic and anti-carcinogenic
effects being reported. The mutagenicity and genotoxicity of areca alkaloids has been
detected by many short-term assays. However, their genotoxicity to oral fibroblasts
and keratinocytes, the target cells of BQ, has not been identified. It would thus
appear that AN toxicity is not completely due to its polyphenol, tannin and alkaloid
content. The single agent which is responsible for AN carcinogenicity awaits further
clarification. Reactive oxygen species produced during auto-oxidation of AN polyphenols
in the BQ-chewer's saliva, are crucial in the initiation and promotion of oral cancer.
Nitrosation of areca alkaloids also produces AN-specific nitrosamines, that have been
demonstrated to be mutagenic, genotoxic and are capable of inducing tumors in experimental
animals. Arecaidine and AN extract are further suggested to be tumor promoters. Antioxidants
such as glutathione and N-acetyl-L-cysteine can potentially prevent such AN-elicited
cytotoxicity. Further studies are needed to delineate the metabolism of AN ingredient
and their roles in the multi-step chemical carcinogenesis, in order to enhance the
success of the future chemoprevention of oral cancer and oral submucous fibrosis.