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  5. Role of areca nut in betel quid-associated chemical carcinogenesis: Current awareness and future perspectives
 
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Role of areca nut in betel quid-associated chemical carcinogenesis: Current awareness and future perspectives

Journal
Oral Oncology
Journal Volume
37
Journal Issue
6
Pages
477-492
Date Issued
2001
Author(s)
JIIANG-HUEI JENG  
Chang M.C.
Hahn L.J.
DOI
10.1016/S1368-8375(01)00003-3
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-0034955131&doi=10.1016%2fS1368-8375%2801%2900003-3&partnerID=40&md5=a72ac409590ab1d9ce86e360c0cd401f
https://scholars.lib.ntu.edu.tw/handle/123456789/570750
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. ? 2001 Elsevier Science Ltd.
Subjects
Areca nut; Arecoline; Betel quid; Chemical carcinogenesis; Nitrosamine; Oral cancer; Oral submucous fibrosis; Reactive oxygen species
SDGs

[SDGs]SDG3

Other Subjects
acetylcysteine; alkaloid derivative; arecaidine; glutathione; nitrosamine; polyphenol derivative; tannin derivative; assay; autooxidation; betel nut; chemical carcinogenesis; chemoprophylaxis; disease association; experimental animal; fibroblast; fibrosis; futurology; genotoxicity; habit; human; keratinocyte; mastication; mouth cancer; mutagenic activity; nitrosation; nonhuman; priority journal; review; saliva; submucosa; target cell
Publisher
Elsevier Ltd
Type
journal article

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