Topic
Arecoline
About: Arecoline is a research topic. Over the lifetime, 744 publications have been published within this topic receiving 16015 citations. The topic is also known as: methylarecaiden & methylarecaidin.
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TL;DR: In the UK, the rate of hospital admission for acute asthma is higher among Asians than among other groups in the population; betel-nut chewing may be one of several factors that affect asthma control and severity of attacks.
72 citations
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TL;DR: Arecoline was concluded to have weak chromosome-damaging effects in vivo, and the frequency of aberrations showed a dose-response relationship.
71 citations
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TL;DR: GAR-3 regulates multiple calcium-dependent processes in the C. elegans pharyngeal muscle through both membrane potential and excitation-contraction coupling, and is associated with membrane depolarization and muscle contraction.
Abstract: Muscarinic acetylcholine receptors regulate the activity of neurons and muscle cells through G-protein-coupled cascades. Here, we identify a pathway through which the GAR-3 muscarinic receptor regulates both membrane potential and excitation-contraction coupling in the Caenorhabditis elegans pharyngeal muscle. GAR-3 signaling is enhanced in worms overexpressing gar-3 or lacking GPB-2, a G-protein beta-subunit involved in RGS-mediated inhibition of G(o)alpha- and G(q)alpha-linked pathways. High levels of signaling through GAR-3 inhibit pharyngeal muscle relaxation and impair feeding--but do not block muscle repolarization--when worms are exposed to arecoline, a muscarinic agonist. Loss of gar-3 function results in shortened action potentials and brief muscle contractions in the pharyngeal terminal bulb. High levels of calcium entry through voltage-gated channels also impair terminal bulb relaxation and sensitize worms to the toxic effects of arecoline. Mutation of gar-3 reverses this sensitivity, suggesting that GAR-3 regulates calcium influx or calcium-dependent processes. Because the effects of GAR-3 signaling on membrane depolarization and muscle contraction can be separated, we conclude that GAR-3 regulates multiple calcium-dependent processes in the C. elegans pharyngeal muscle.
70 citations
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TL;DR: Stress caused by long-term ANE exposure enhances oxidative stress and genetic damage in human keratinocytes, and intracellular antioxidative activity may also be enhanced in response to increased oxidative stress.
Abstract: Chewing betel quid (BQ) is a popular habit worldwide A causal association between BQ chewing and oral cancer has been well documented Emerging evidence indicates that sustained exposure to stress induces epigenetic reprogramming of some mammalian cells and increases the mutation rate to accelerate adaptation to stressful environments In this study, we first confirmed that 24-h treatment with areca nut extracts (ANE; a major component of BQ) at doses over 40 μg/ml induced mutations at the hypoxanthine phosphoribisyltransferase ( HPRT ) locus in human keratinocytes (HaCaT cells) We then investigated whether the stress of long-term exposure to sublethal doses of ANE (0, 5 and 20 μg/ml for 35 passages) could enhance genetic damage to HaCaT cells Compared to cells exposed to 0 or 5 μg/ml ANE, cells exposed to 20 μg/ml ANE were slightly but significantly more resistant to a 72-h treatment with ANE and its major ingredients, arecoline and arecaidine, but did not develop cross-resistance to other BQ ingredients or alcohol The cells that received 20 μg/ml ANE for 35 passages also had a significantly increased mutation frequency at the HPRT locus and an increased frequency in the appearance of micronuclei compared to lower doses Moreover, increased intracellular levels of reactive oxygen species and 8-hydroxyguanosine in cells exposed to 20 μg/ml ANE suggested that long-term ANE exposure results in the accumulation of oxidative damage However, cells subjected to long-term treatment of 20 μg/ml ANE contained higher levels of glutathione than unexposed cells Therefore, after long-term exposure to sublethal doses of ANE, intracellular antioxidative activity may also be enhanced in response to increased oxidative stress These results suggest that stress caused by long-term ANE exposure enhances oxidative stress and genetic damage in human keratinocytes
70 citations
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TL;DR: Reaction between arecoline and glutathione or N-acetyl-l-cysteine occurred maximally at neutral pH and decreased rapidly with increasing acidity, indicating that reaction between un-ionized species occurred more readily than nucleophilic addition (Ad(N)) reactions involving charged intermediates.
Abstract: 1 In the rat, arecoline is converted into arecaidine and both compounds are converted into N-acetyl-S-(3-carboxy-1-methylpiperid-4-yl) -l-cysteine 2 The structure of the metabolite was established by (a) synthesis, (b) conversion into N-acetyl-S-(3-methoxycarbonyl-1-methylpiperid-4-yl) -l-cysteine methyl ester, which was chromatographically identical with the synthetic material, and (c) nmr-and ir-spectral analysis of the 3-methoxycarbonyl derivative 3 In ethanolic solution, or in phosphate buffer at pH7·0, arecoline reacted with N-acetyl-l-cysteine to give N-acetyl-S-(3-methoxycarbonyl-1-methylpiperid-4-yl) -l-cysteine; under similar conditions, arecaidine reacted more slowly to give N-acetyl-S-(3-carboxy-1-methylpiperid-4-yl) -l-cysteine 4 The reaction between arecoline and glutathione or N-acetyl-l-cysteine occurred maximally at neutral pH and decreased rapidly with increasing acidity At neutral pH, the reactions were bimolecular and second-order when the reactants were in approximately equimolar concentrations and pseudo-unimolecular first-order when arecoline was in large excess 5 Consideration of the pKa values and degrees of ionization of the reactants and the effect of pH on the stoicheiometry of reaction between arecoline and glutathione or N-acetyl-l-cysteine indicated that reaction between un-ionized species occurred more readily than nucleophilic addition (AdN) reactions involving charged intermediates
69 citations