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: A review of the available evidence on the carcinogenicity of AN based on the findings reported in the recently published experimental studies is discussed in the present review as mentioned in this paper , which includes cellular and molecular effects induced by AN, including promoting epithelial-mesenchymal transition, autophagy initiation, tissue hypoxia, genotoxicity, cytotoxicity and cell death.
Abstract: Oral cancers (OC) are among the most frequent malignancies encountered in Southeast Asia, primarily due to the prevalent habit of betel quid (BQ) and smokeless tobacco use in this region. Areca nut (AN), the primary ingredient in BQ, contains several alkaloids, including arecoline, arecaidine, guvacoline, and guvacine. These have been associated with both the AN abuse liability and carcinogenicity. Additionally, variations in AN alkaloid levels could lead to differences in the addictiveness and carcinogenic potential across various AN-containing products. Recent studies based on animal models and in vitro experiments show cellular and molecular effects induced by AN. These comprise promoting epithelial-mesenchymal transition, autophagy initiation, tissue hypoxia, genotoxicity, cytotoxicity, and cell death. Further, clinical research endorses these undesired harmful effects in humans. Oral submucosal fibrosis, a potentially malignant disease of the oral cavity, is predominantly reported from the geographical areas of the globe where AN is habitually chewed. OC in chronic AN users presents a more aggressive phenotype, such as resistance to anti-cancer drugs. The available evidence on the carcinogenicity of AN based on the findings reported in the recently published experimental studies is discussed in the present review.
1 citations
TL;DR: Xanomeline demonstrated functional selectivity for M1 receptors when tested in isolated tissue preparations and in cloned cell lines expressing specific muscarinic receptor subtypes.
1 citations
TL;DR: Wang et al. as discussed by the authors comprehensively provided bibliometric characteristics of all the papers on betel quid (BQ)-related cancer and precancerous lesions published until 2022 in the Scopus database.
1 citations
TL;DR: Acetylcholine-induced response was inhibited by both cholinoblockers more or less equally and selective desensitization of receptors by nicotine and muscarine as well as receptor occupancy by cytisine and arecoline reduced acetylchloline- induced response.
Abstract: Cholinoreceptors were identified at the somatic membrane of theHelix lucorum RPa4 neuron using intracellular recording techniques. Application of specific agonists of nicotinic (nicotine, cytisine) and muscarinic (muscarine, arecoline) cholinoreceptors to the soma produced neuronal depolarization. The depolarization produced by applying acetylcholine to the cell was of short duration and was often replaced by hyperpolarization. Both selective desensitization of receptors by nicotine and muscarine as well as receptor occupancy by cytisine and arecoline reduced acetylchloline-induced response. The nicotinic cholinoblocker d-tubocurarine substantially inhibited responses to nicotinic cholinomimetics, while atropine, a muscarinic cholinoblocker, depressed response to muscarinic cholinomimetics. Acetylcholine-induced response was inhibited by both cholinoblockers more or less equally. The presence at the RPa4 neuronal somatic membrane is postulated of standard nicotinic and muscarinic cholinoreceptors similar to those found in vertebrates.
1 citations