Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Areca”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

Effects of areca nut on growth, differentiation and formation of DNA damage in cultured human buccal epithelial cells.

Because the high incidence of oral cancers in South-East Asia is causally linked to the common habit of betel quid chewing, the effects of an aqueous extract of areca nut, one of the main ingredients of the quid, on growth, differentiation, morphology and DNA damage were studied in cultured human buccal epithelial cells. An acute exposure (3 hr) of the cells to the extract altered their morphology and induced ridges in the plasma membrane, with indications of internalization of extract particles. Such exposure also caused formation of DNA single-strand breaks which accumulated during post-treatment culture, indicating continuous exposure to residual particles and/or the possibility of inhibited DNA repair. The extract accelerated terminal differentiation of the cells, measured as involucrin expression at relatively non-toxic levels. The extract caused similar loss of colony-forming efficiency in normal cells and in a buccal carcinoma cell line (SqCC/YI) which was defective in its ability to undergo differentiation, indicating that extract toxicity could occur independently from this response. Finally, the genotoxicity of the salivary areca-nut-specific carcinogen 3-(N-nitrosomethyl-amino)propionaldehyde, was demonstrated by the formation of DNA protein cross-links and DNA single-strand breaks in normal buccal epithelial cells. These findings in vitro suggest that betel quid carcinogenesis in the human oral cavity may involve cytopathic alterations of normal cell morphology, growth and differentiation, as well as formation of DNA damage by areca-nut-related agents extracted or formed in saliva.

Areca↗

The association between microsomal epoxide hydrolase genotypes and esophageal squamous-cell-carcinoma in Taiwan: interaction between areca chewing and smoking.

One hundred and forty-five ESCC patients and 352 controls were recruited from three hospitals in Taiwan to determine the association between esophageal squamous-cell-carcinoma (ESCC) and microsomal epoxide hydrolase (mEH) genotypes at Thy113His and His139Arg. Stratified by their exposures, the His113His genotype was a significant protective factor for ESCC in areca chewers and tobacco smokers. Stratified by His113 polymorphisms, the risk of contracting ESCC for participants with His113His who chewed areca and smoked was >50% less than for those with Thy113Thy. We suggest that the mEH His113His genotype can differentiate the association between smoking, areca chewing, and ESCC.

Adult↗

Areca nut extract treatment down-regulates involucrin in normal human oral keratinocyte through P13K/AKT activation.

Areca (betel) is an important etiological factor linked to the high prevalence of oral carcinoma and other oral diseases in South Asians. Involucrin is a key component of the cornified envelop and a differentiation marker of keratinocyte. In this study, we found that 5 microg/ml non-toxic areca nut extract (ANE) treatment resulted in the 0.5-fold down-regulation of involucrin and disruption in involucrin distribution in normal human oral keratinocyte (NHOK). Progressive down-regulation of involucrin during oral carcinogenesis was noted. Activation of AKT by 1.7-fold and up-regulation of COX-2 by 2-fold were elicited following ANE treatment in NHOK. Treatment with PI3K/AKT blockers reverted the down-regulation of involucrin. ANE also down-regulated involucrin by 0.6-fold and disturbed both cornified envelope and cell aggregation in calcium-induced differentiated NHOK. However, such phenomena seemed to be independent from the ANE-associated COX-2 activation. The ANE-associated down-regulation of involucrin through AKT pathway could underlie the areca-associated epithelial pathogenesis.

Adult↗

Oxidative damage to DNA induced by areca nut extract.

In Taiwan, people chew betel quid which contains tender areca nut with husk. In other countries, people prefer ripe and dried areca nut without husk. In this study, we compared the reactive oxygen species-induced oxidative DNA damage in isolated DNA and CHO-K1 cells between treatments with tender areca nut extract (ANE) and ripe ANE. Incubation of these two ANE preparations with isolated DNA generated 8-hydroxy-2'-deoxyguanosine (8-OH-dG) in an alkaline environment in a dose-dependent manner. Ripe ANE generated higher levels of 8-OH-dG compared to tender ANE. The addition of iron(II) (100 microM) resulted in 1.4- and 3.1-fold increases of 8-OH-dG when incubated with 1 mg/ml each of tender and ripe ANE. In testing the effect of ANE to cellular DNA, CHO-K1 cells were used for its documented sensitivity to reactive oxygen species. In CHO-K1 cells, ripe ANE was more cytotoxic than tender ANE following an 18-h incubation. The cytotoxicity to CHO-K1 cells was positively correlated with the formation of 8-OH-dG following tender (r=0.97) and ripe (r=0.91) ANE treatment. Addition of the iron chelating agent o-phenanthroline (10 and 20 microM) to cells prior to ri ANE exposure significantly increased (p<0.05) the survival of CHO-K1 cells. In addition, ripe ANE induced dichlorofluorescein-mediated fluorescence which indicated the formation of hydrogen peroxide in CHO-K1 cells. In conclusion, this study demonstrated that ANE-induced oxidative damage to isolated and cellular DNA which may result from the generation of hydrogen peroxide, and iron may serve as a catalyst in this process. Furthermore, ripe ANE generated higher oxidative DNA damage levels compared to tender ANE.

8-Hydroxy-2'-Deoxyguanosine↗

A metabolomic approach to the metabolism of the areca nut alkaloids arecoline and arecaidine in the mouse.

The areca alkaloids comprise arecoline, arecaidine, guvacoline, and guvacine. Approximately 600 million users of areca nut products, for example, betel quid chewers, are exposed to these alkaloids, principally arecoline and arecaidine. Metabolism of arecoline (20 mg/kg p.o. and i.p.) and arecaidine (20 mg/kg p.o. and i.p.) was investigated in the mouse using a metabolomic approach employing ultra-performance liquid chromatography-time-of-flight mass spectrometric analysis of urines. Eleven metabolites of arecoline were identified, including arecaidine, arecoline N-oxide, arecaidine N-oxide, N-methylnipecotic acid, N-methylnipecotylglycine, arecaidinylglycine, arecaidinylglycerol, arecaidine mercapturic acid, arecoline mercapturic acid, and arecoline N-oxide mercapturic acid, together with nine unidentified metabolites. Arecaidine shared six of these metabolites with arecoline. Unchanged arecoline comprised 0.3-0.4%, arecaidine 7.1-13.1%, arecoline N-oxide 7.4-19.0%, and N-methylnipecotic acid 13.5-30.3% of the dose excreted in 0-12 h urine after arecoline administration. Unchanged arecaidine comprised 15.1-23.0%, and N-methylnipecotic acid 14.8%-37.7% of the dose excreted in 0-12 h urine after arecaidine administration. The major metabolite of both arecoline and arecaidine, N-methylnipecotic acid, is a novel metabolite arising from carbon-carbon double-bond reduction. Another unusual metabolite found was the monoacylglyceride of arecaidine. What role, if any, that is played by these uncommon metabolites in the toxicology of arecoline and arecaidine is not known. However, the enhanced understanding of the metabolic transformation of arecoline and arecaidine should contribute to further research into the clinical toxicology of the areca alkaloids.

Animals↗

Cyclin D1 genotype in areca-associated oral squamous cell carcinoma.

BACKGROUND: Oral squamous cell carcinoma (OSCC) is the most common malignancy in areca-chewing regions, accounting for up to 50% of malignant tumors in some South Asian countries. Amplification and/or over-expression of cyclin D1 (CCND1) is a frequent event in human malignancies, including OSCC. CCND1 G870A polymorphism (codon 242) gives rise to two isoforms of the protein. The objective of the present study was to evaluate if the risk, onset, and prognosis of areca-associated OSCC is related to CCND1 genotypes. METHODS: We analyzed the CCND1 genotype in 70 OSCC cases and 93 control Taiwanese using single-strand conformation polymorphism techniques. RESULTS: Statistical analysis showed that CCND1 genotype had no impact on the risk, onset, or survival of areca-associated OSCC. However, buccal squamous cell carcinoma (BSCC) appeared to be less frequently associated with AA genotype than non-BSCC (P = 0.02). In addition, amplification of CCND1 was significantly more prevalent in OSCC cases (22%) than in control subjects (2%, P < 0.01). CONCLUSION: This study demonstrates that the CCND1 genotype may confer different risks for BSCC and non-BSCC.

Adult↗

Modulation of KGF-1 gene expression in oral fibroblasts by ripe areca nut extract.

BACKGROUND: Areca chewing is a common habit of Asians, leading to a high propensity for a variety of oral diseases in this population. This research aimed to study the expression level of genes in oral fibroblast cell lines in response to exposure to ripe areca nut extract (rANE). METHODS: Fifteen oral fibroblast cell lines obtained from individuals aged 20-77 years were established. Treatment of a cell line with 40 micro g/ml rANE for 24 h was performed to achieve RNA for cDNA microarray analysis. RESULTS: Among some 320 genes exhibiting detectable expression levels, 14 were up-regulated and 26 were down-regulated more than 2.5-fold. Semi-quantitative RT-PCR analysis suggested that up-regulation of IL-6 expression and down-regulation of PDGFR, APP-1 and KGF-1 expressions in multiple cell lines assayed, were compatible with the results of the microarray analysis. Using quantitative real-time RT-PCR analysis, a remarkable down-regulation of KGF-1 expression in response to 40 microg/ml rANE, ranging 1.5-ninefold as compared to controls, was found in 60% (9/15) of the cell lines. CONCLUSION: This study established a novel toxicogenomic database for rANE. The down-regulation of KGF-1 expression in oral fibroblast cell lines potentially impairs the proliferation of overlying keratinocytes, which could partially explain the frequent epithelial atrophy observed in chronic areca chewers in vivo.

Adult↗

Sociocultural aspects of areca nut use.

This paper aims to describe the sociocultural context of areca nut use through exploring people's norms and values and the meaning underlying a wide range of different practices. A historical review is followed by an examination of more recent evidence, including quantitative and qualitative research conducted in the United Kingdom. It is concluded that some reports involving the various uses of areca nut and the conclusions drawn are confusing and that future studies need to be more explicit. While a sound scientific background is required, important sociocultural and religious issues around areca nut use must also be understood if health promotion initiatives are to be considered.

Africa↗

Chemical and analytical aspects of areca nut.

A capillary zone electrophoretic (CZE) method for the rapid analysis of the major alkaloids (arecoline and guavacoline) in areca nut extract is described. Areca nuts were pulverized and then extracted with water by sonication in a water bath. After centrifugation, the supernatant was analysed on a fused-silica capillary with 100 mM ammonium acetate-acetic acid (pH 4.6) as the running buffer at a voltage of 20 kV and temperature of 30 degrees C. The method is applicable to the analysis of alkaloids in the nut, commercial preparations (pan masala) and in the saliva of areca nut chewers.

Alkaloids↗

Ingredients contribute to variation in production of reactive oxygen species by areca quid.

Areca quid (AQ) chewing has been implicated an independent risk factor for the development of oral cancer. Taiwanese areca quid (AQ) refers to a combination of areca nut (AN), lime, and inflorescence of Piper betle Linn. (IPB) or Piper betle leaf (PBL). Studies of AQ in other countries reported that AN extract combined with lime generates reactive oxygen species (ROS), such as hydroxyl radical (HO.), known to be a contributing factor in oral mucosa damage. To determine whether HO. is formed in the oral cavity during AQ chewing, the formation of meta-tyrosine (m-Tyr) and ortho-tyrosine (o-Tyr) from l-phenylalanine (Phe) was confirmed. It was demonstrated that combined aqueous extracts of AN, lime, metal ions (such as Cu2+ and Fe2+), and IPB or PBL produced HO.. Thus, the yield of HO. significantly increases when higher amounts of IPB or lime are added and also when Cu2+ and Fe2+ are increased. Further, the omission of any one of these ingredients significantly reduces the formation of HO.. Our results found that chewing AQ with IPB generated significantly higher HO. than chewing AQ with PBL, and may result in greater oxidative damage to the surrounding oral mucosa.

Adult↗

Etiology of oral submucous fibrosis with special reference to the role of areca nut chewing.

Oral submucous fibrosis (OSF) is a high risk precancerous condition, predominantly affecting Indians. Consumption of chilli was hypothesized as an etiologic factor on the basis of ecological observations and a solitary animal experimental study. Subsequent epidemiologic studies that included case-series reports, large cross-sectional surveys, case-control studies, cohort and intervention studies have identified areca nut as the major etiologic agent. Tissue-culture studies involving human fibroblasts, areca nut extracts and areca nut alkaloids supported this etiologic hypothesis by showing fibroblastic proliferation and increased collagen formation. Currently, the role of genetic susceptibility and that of autoimmunity are receiving attention. The influence of nutritional factors, if any, remains unclear.

Animals↗

The molecular markers for prognostic evaluation of areca-associated buccal squamous cell carcinoma.

BACKGROUND: Buccal squamous cell carcinoma (BSCC) is the most frequently occurring oral cancer in Asians due to the popularity of areca use in this area. The aim of the present study was to evaluate the survival of areca-associated BSCC associated with multiple molecular markers. METHODS: Using immunohistochemistry, we evaluated the survival of a cohort of 55 patients with BSCC being followed long term, as correlated to the expression of variable markers. RESULTS: We found that p53, p21, Rb, cyclin D1 (CCD1), MDM2, and gamma-catenin were positive in 81, 60, 70, 31, 88, and 44% of patients, respectively. Subjects with -ve immunoreactivity for CCD1, and +ve immunoreactivity for MDM2 and gamma-catenin had significantly better survival than subjects with the opposite immunoreactive pattern. KAPLAN-meier survival curves confirmed this association. CONCLUSION: The data indicate that expression of CCD1, MDM2, and gamma-catenin might serve as potential prognostic markers for BSCC in areca-using patients.

Adult↗

Areca-nut abuse and neonatal withdrawal syndrome.

Areca-nut chewing occurs widely in South Asia and the Indian subcontinent. Here we present a case of neonatal withdrawal syndrome in an infant born to a woman who was a chronic areca-nut user. Arecoline, the principal neuroactive alkaloid in areca nuts, was found in the mother's placenta.

Adult↗

Treatment of experimental heterophyiasis with two plant extracts, areca nut and pumpkin seed.

The effect of water extracts of areca nut and pumpkin seeds in the treatment of puppies experimental infected with heterophyiasis gave promising results. Puppies were infected through feeding on the muscles of Mugil sp. fish containing the encysted metacercariae of H. heterophyes. Decoctions of pumpkin seeds and areca nut were administered orally 2 weeks after the start of infection as indicated by positive stool examinations. The effect was evaluated by stool examination for eggs, and by autopsy for worms in the intestines. A combined extracts of areca nut and pumpkin seeds gave an excellent result than when given either extract alone.

Animals↗

[Research on inhibition of areca nut extract on human buccal keratinocytes].

OBJECTIVE: To culture human oral mucosa epithelial cells in vitro and study the mechanism of changes in the epithelia of oral submucous fibrosis (OSF). METHODS: The keratinocytes were obtained from normal buccal mucosa (NM-KC) and OSF buccal mucosa (OSF-KC) with dispase trypsine and cultured in vitro. Then the cell proliferation of keratinocytes incubated with or without areca nut extract in the presence of 10% fetal calf serum for 48 hours at 37 degrees C in 5% CO2 and air were monitored by use of thiazolyl blue (MTT) assay. RESULTS: Primary culture grew in small islands that coalesced at confluency. Ultrastructurally the cells contained a large of tonofilament and microvilli. Immunohistochemistry demonstrated uniform staining of the cells with antibodies to keratins. There was no difference in cell proliferation between OSF-KC and NM-KC, and areca nut extract inhibited keratinocyte proliferation in a concentration-dependent manner. CONCLUSION: The results suggested that utilizing dispase II can establish fibroblast-free culture for growing of human oral mucosa keratinocytes and areca nut extract is a cytotoxic agent to human buccal keratinocytes.

Areca↗

Areca-nut toxicity in cultured human buccal epithelial cells.

In cultured human buccal epithelial cells, at doses of 3-540 micrograms/ml, areca-nut extract significantly decreased viability, as determined by colony-forming efficiency, clonal growth rate, ability to take up neutral red and ability to exclude trypan blue, and also caused significant formation of DNA single-strand breaks and DNA protein cross-links. Comparisons of the areca nut-related compounds, 3-(N-nitrosomethylamino)propion-aldehyde (NMPA), 3-(N-nitrosomethylamino)propionitrile (NMPN), N-nitrosoguvacoline, N-nitrosoguvacine, arecoline, arecaidine, guvacoline and guvacine, in terms of the above endpoints, indicate that NMPA is ten times more cytopathic to buccal cells than the other agents on a molar basis. Because metabolism of NMPA can potentially yield several reactive breakdown products, including aldehydes, this study indicates that both the parent compound and its metabolites may contribute to the observed pathobiological effects. Taken together, the observed pathobiological effects of areca-nut extract and certain related compounds in cultured human buccal epithelial cells indicate that these agents may contribute to the oral carcinogenicity associated with chewing betel quid.

Areca↗

Copy number amplification of 3q26-27 oncogenes in microdissected oral squamous cell carcinoma and oral brushed samples from areca chewers.

Oral squamous cell carcinoma (OSCC) is a worldwide disease. In South Asians, the high prevalence of OSCC is tightly linked to areca chewing. The prognosis for OSCC remains dismal and improvement in early diagnosis may benefit the survival of patients with this disease. Chromosome region 3q26-27 has been shown to carry several oncogenes. By quantitative PCR (Q-PCR), the gene copy numbers of TERC, PI3KCA, ZASC1, and TP63 from microdissected OSCCs have been determined. Copy number amplifications of PI3KCA and ZASC1, a newly identified zinc finger transcription factor, were identified in 30 (65%) and 32 (70%) of 46 primary OSCCs, respectively. Co-amplification of PI3KCA and ZASC1 in 50% of primary OSCCs suggests that they are critical targets of the 3q26.3 amplicon. OSCCs carrying higher levels of PI3KCA and/or ZASC1 copy number amplification were associated with a significantly higher propensity for lymph node metastasis. ZASC1 mRNA expression in OSCC was also associated with lymph node metastasis. In addition, copy number amplification of at least one 3q26-27 oncogene was detected in brush samples from 10 of 22 (45%) patients with oral leukoplakia and 5 of 20 (25%) oral mucosa samples from areca chewers without a visible lesion. These data indicate frequent copy number amplification and overexpression of ZASC1 in OSCC. The findings also suggest the potential use of Q-PCR analysis and brush collection of samples to dissect OSCC risk.

Adult↗

Effect of areca nut on salivary copper concentration in chronic chewers.

The chewing of areca nut is associated with the development of oral submucous fibrosis (OSF), a condition predominantly encountered in Asians indulging in the habit. The pathogenesis of this condition is however, unclear, though several mechanisms have been proposed. Copper has previously been implicated as a possible aetiological factor. In this study, total copper concentration was measured via atomic absorption spectrophotometry in whole mouth saliva of 15 volunteers who were regular chewers, before and after their habitual chew. An aliquot of the latter was also analysed for copper. Six non-chewing volunteers acted as controls. Salivary copper concentrations were corrected for protein content. Over 50% of the subjects had basal salivary copper concentration higher than the range seen in normal controls. All but two subjects demonstrated an increase in the salivary [Cu] following their habitual chew. Marked changes were seen in those with low basal salivary concentrations. These data indicate that soluble copper found in areca nut is released into the oral environment of habitual chewers. Its buccal absorption may contribute to the oral fibrosis in Asians who regularly chew this nut.

Adolescent↗