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Journal ArticleDOI

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

Jiiang-Huei Jeng, +2 more
- 01 Sep 2001 - 
- Vol. 37, Iss: 6, pp 477-492
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TLDR
It would appear that AN toxicity is not completely due to its polyphenol, tannin and alkaloid content, and further studies are needed to delineate the metabolism of AN ingredient and their roles in the multi-step chemical carcinogenesis, to enhance the success of the future chemoprevention of oral cancer and oral submucous fibrosis.
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This article is published in Oral Oncology.The article was published on 2001-09-01. It has received 382 citations till now. The article focuses on the topics: Oral submucous fibrosis & Areca.

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Citations
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Journal ArticleDOI

The oral health consequences of chewing areca nut.

TL;DR: There is new information linking oral cancer to pan chewing without tobacco, suggesting a strong cancer risk associated with this habit and public health measures to quit areca use are recommended to control disabling conditions such as submucous fibrosis and oral cancer among Asian populations.
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Stimulation of glutathione depletion, ROS production and cell cycle arrest of dental pulp cells and gingival epithelial cells by HEMA.

TL;DR: HEMA-induced growth inhibition in HPF and S-G cells in a dose-dependent manner, which may be partially explained by induction of cell cycle perturbation, helped to define the mechanism of the cytotoxicity caused by HEMA.
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Molecular genetics of premalignant oral lesions.

TL;DR: This review summarizes the investigation of the molecular genetics of each of the histologically distinct lesions of the oral cavity and relates them to the alterations, which have been demonstrated in OSCC, to define their location on the continuum of changes, which lead to malignant transformation.
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Areca catechu L. (Arecaceae): a review of its traditional uses, botany, phytochemistry, pharmacology and toxicology.

TL;DR: As an important herbal medicine, A. catechu has potential for the treatment of many diseases, especially parasitic diseases, digestive function disorders, and depression, and further research should be undertaken to investigate the clinical effects, toxic constituents, target organs, and pharmacokinetics.
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Roles of keratinocyte inflammation in oral cancer: regulating the prostaglandin E2, interleukin-6 and TNF-α production of oral epithelial cells by areca nut extract and arecoline

TL;DR: The results indicate that BQ chewing contributes to the pathogenesis of cancer and OSF by impairing T cell activation and by induction of PGE2, TNF-alpha and IL-6 production, which affect oral mucosal inflammation and growth of OMF and oral epithelial cells.
References
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Journal ArticleDOI

Prooxidant states and tumor promotion.

Peter A. Cerutti
- 25 Jan 1985 - 
TL;DR: Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents.
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Insertion of specific bases during DNA synthesis past the oxidation-damaged base 8-oxodG.

TL;DR: DCMP and dAMP are incorporated selectively opposite 8-oxodG with transient inhibition of chain extension occurring 3' to the modified base, and the potentially mutagenic insertion of dAMP is targeted exclusively to the site of the lesion.
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Oxyradicals and DNA damage

TL;DR: The levels of oxidative DNA damage reported in many human tissues or in animal models of carcinogenesis exceed the levels of lesions induced by exposure to exogenous carcinogenic compounds, and it seems likely that oxidativeDNA damage is important in the etiology of many human cancers.
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Apoptosis in cancer

TL;DR: An intense research effort is uncovering the underlying mechanisms of apoptosis such that, in the next decade, one envisions that this information will produce new strategies to exploit apoptosis for therapeutic benefit.
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Free radicals as mediators of tissue injury and disease.

TL;DR: This review discusses cellular sources of various radical species and their reactions with vital cellular constituents to provide insights into the controversy over whether free radicals are important mediators of tissue injury.
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