About: Arecoline is a(n) research topic. Over the lifetime, 744 publication(s) have been published within this topic receiving 16015 citation(s). The topic is also known as: methylarecaiden & methylarecaidin.
Papers published on a yearly basis
01 Jul 2006-Oral Oncology
TL;DR: Current evidence implicates collagen-related genes in the susceptibility and pathogenesis of OSF and the individual mechanisms operating at various stages of the disease-initial, intermediate and advanced need further study in order to propose appropriate therapeutic interventions.
Abstract: Data from recent epidemiological studies provide overwhelming evidence that areca nut is the main aetiological factor for OSF. A clear dose-dependent relationship was observed for both frequency and duration of chewing areca nut (without tobacco) in the development of OSF. Commercially freeze dried products such as pan masala, Guthka and mawa (areca and lime) have high concentrates of areca nut per chew and appear to cause OSF more rapidly than by self prepared conventional betel quid that contain smaller amounts of areca nut. It is logical to hypothesise that the increased collagen synthesis or reduced collagen degradation as possible mechanisms in the development of the disease. There are numerous biological pathways involved in the above processes and, it is likely that the normal regulatory mechanisms are either down regulated or up regulated at different stages of the disease. Among the chemical constituents, alkaloids from areca nut are the most important biologically whilst tannin may have a synergistic role. These chemicals appear to interfere with the molecular processes of deposition and/or degradation of extracellular matrix molecules such as collagen. In vitro studies on human fibroblasts using areca extracts or chemically purified arecoline support the theory of fibroblastic proliferation and increased collagen formation that is also demonstrable histologically in human OSF tissues. The copper content of areca nut is high and the possible role of copper as a mediator of fibrosis is supported by the demonstration of up regulation of lysyl oxidase in OSF biopsies. It has been postulated that areca nut may also induce the development of the disease by increased levels of cytokines in the lamina propria. Increased and continuous deposition of extracellular matrix may take place as a result of disruption of the equilibrium between matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMP). Current evidence implicates collagen-related genes in the susceptibility and pathogenesis of OSF. The individual mechanisms operating at various stages of the disease-initial, intermediate and advanced-need further study in order to propose appropriate therapeutic interventions.
01 Sep 2001-Oral Oncology
TL;DR: 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.
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.
01 Sep 1972-Neuropharmacology
TL;DR: Bilateral injection of atropine into the caudate-putamen and globus pallidus did not modify the catalepsy induced by peripheral administration of haloperidol or arecoline but intranigral atropines markedly potentiated the cataleptic effects of these drugs.
Abstract: Haloperidol, arecoline and atropine were injected in various combinations into the caudate-putamen, globus pallidus and substantia nigra. Unilateral injections of haloperidol or arecoline into the caudate-putamen, globus pallidus or substantia nigra induced an ipsilateral circling behaviour, the globus pallidus being the most sensitive and the substantia nigra the least sensitive to this effect. Atropine induced a contralateral circling behaviour after injection into the caudate-putamen or globus pallidus and in each case potentiated the ipsilateral circling of haloperidol and arecoline when injected into the opposite nucleus. The injection of atropine into the same caudate-putamen as haloperidol or arecoline inhibited the ipsilateral circling induced by the latter drugs. Catalepsy was observed after haloperidol injections into the caudate-putamen and globus pallidus, the latter nucleus being the most sensitive. Catalepsy was not observed after arecoline injection into any of the nuclei considered. The bilateral injection of atropine into the caudate-putamen and globus pallidus did not modify the catalepsy induced by peripheral administration of haloperidol or arecoline but intranigral atropine markedly potentiated the cataleptic effects of these drugs. Results are discussed in terms of cholinergic and dopaminergic mechanisms within the extrapyramidal system.
TL;DR: Results suggest that betel chewing mainly affects the central and autonomic nervous systems, and may affect parasympathetic, GABAnergic and sympathetic functions.
Abstract: Betel chewing has been claimed to produce a sense of well-being, euphoria, heightened alertness, sweating, salivation, a hot sensation in the body and increased capacity to work. Betel chewing also leads to habituation, addiction and withdrawal. However, the mechanisms underlying these effects remain poorly understood. Arecoline, the major alkaloid of Areca nut, has been extensively studied, and several effects of betel chewing are thought to be related to the actions of this parasympathomimetic constituent. However, betel chewing may produce complex reactions and interactions. In the presence of lime, arecoline and guvacoline in Areca nut are hydrolyzed into arecaidine and guvacine, respectively, which are strong inhibitors of GABA uptake. Piper betle flower or leaf contains aromatic phenolic compounds which have been found to stimulate the release of catecholamines in vitro. Thus, betel chewing may affect parasympathetic, GABAnergic and sympathetic functions. Betel chewing produces an increase in heart rate, blood pressure, sweating and body temperature. In addition, EEG shows widespread cortical desynchronization indicating a state of arousal. In autonomic function tests, both the sympathetic skin response and RR interval variation are affected. Betel chewing also increases plasma concentrations of norepinephrine and epinephrine. These results suggest that betel chewing mainly affects the central and autonomic nervous systems. Future studies should investigate both the acute and chronic effects of betel chewing. Such studies may further elucidate the psychoactive mechanisms responsible for the undiminished popularity of betel chewing since antiquity.
01 Jan 1986-Archives of Oral Biology
TL;DR: Fibroblasts are responsive to the major metabolite of arecoline and hydrolysis of the ester group may be necessary for this action, which may contribute to the accumulation of collagen in OSF.
Abstract: Oral submucous fibrosis (OSF) is characterized by excessive collagen production by mucosal fibroblasts and is associated with the habitual chewing of betel-nuts (Areca catechu); nut extracts stimulate fibroblast activity in vitro. The metabolism of arecoline, the major alkaloid in the nut, by human buccal mucosa fibroblasts in vitro was investigated; alkaloid metabolites extracted from culture media were analysed by gas chromatography and thin-layer chromatography. [3H]-arecoline was metabolized predominantly to [3H]-arecaidine and this was accompanied by a concentration-dependent stimulation of collagen synthesis and cell proliferation. Arecaidine was a more potent stimulator than arecoline. The rate of hydrolysis of a series of synthetic arecaidine esters (methyl, ethyl, butyl, propyl and pentyl) by fibroblasts was closely correlated with the extent of stimulation of collagen synthesis. Thus fibroblasts are responsive to the major metabolite of arecoline and hydrolysis of the ester group may be necessary for this action. Exposure of buccal mucosa fibroblasts to these alkaloids in vivo may contribute to the accumulation of collagen in OSF.
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