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.

Elevated Snail Expression Mediates Tumor Progression in Areca Quid Chewing-Associated Oral Squamous Cell Carcinoma via Reactive Oxygen Species

Abstract: Background Snail is an important transcription factor implicated in several tumor progression and can be induced by reactive oxygen species (ROS) Areca quid chewing is a major risk factor of oral squamous cell carcinoma (OSCC) Therefore, we hypothesize that the major areca nut alkaloid arecoline may induce Snail via ROS and involve in the pathogenesis of areca quid chewing-associated OSCC

Potential action of betel alkaloids on positive and negative symptoms of schizophrenia: a review.

Abstract: Background: The Areca catechu Linn. is the fourth most used drug in the world after nicotine, ethanol and caffeine. This plant contains nine alkaloids with muscarinic and nicotinic action, which could have an antipsychotic effect. Aim: The aim of this work is reviewing literature data about the potential action of betel alkaloids on positive, negative and cognitive symptoms of schizophrenia. Method: We reviewed the clinical literature data since 1980 via a PubMed search for the terms: arecoline, arecaidine, guvacine, guvacoline, betel, Areca catechu, positive and negative symptoms, cognitive symptoms, psychosis and schizophrenia in combination. Conclusion: Male high consumption of betel had significantly lower positive symptoms than low consumers or non-betel users.

Effects of nicotinic and muscarinic compounds on biting attack in the cat.

Abstract: Predatory-like biting attack on a rat, as well as hissing, growling, and other threat behaviors, could be induced in normally non-aggressive cats by systemic administration of the muscarinic agonist, arecoline (7–12 mg/kg). In contrast to arecoline, nicotine was found to suppress aggressive behaviors. Systemic administration of nicotine (0.5 mg/kg) prior to arecoline injection resulted in a significant reduction in elicited attack and threat behaviors. Furthermore, nicotine (0.075–0.500 mg/kg) was found to produce a dose-dependent suppression of natural predatory behavior as well. This nicotine-produced suppression of attack did not appear to be due to the induction of general malaise, since attack suppression could be seen in the absence of general behavioral inhibition, and doses of nicotine resulting in complete suppression of attack had little effect on food intake. Results indicate that muscarinic and nicotinic compounds can exert antagonistic control over some types of aggressive behaviors.

Areca nut components stimulate ADAM17, IL-1α, PGE2 and 8-isoprostane production in oral keratinocyte: role of reactive oxygen species, EGF and JAK signaling.

Abstract: Betel quid (BQ) chewing is an etiologic factor of oral submucous fibrosis (OSF) and oral cancer. There are 600 million BQ chewers worldwide. The mechanisms for the toxic and inflammatory responses of BQ are unclear. In this study, both areca nut (AN) extract (ANE) and arecoline stimulated epidermal growth factor (EGF) and interleukin-1α (IL-1α) production of gingival keratinocytes (GKs), whereas only ANE can stimulate a disintegrin and metalloproteinase 17 (ADAM17), prostaglandin E2 (PGE2) and 8-isoprostane production. ANE-induced EGF production was inhibited by catalase. Addition of anti-EGF neutralizing antibody attenuated ANE-induced cyclooxygenase-2 (COX-2), mature ADAM9 expression and PGE2 and 8-isoprostane production. ANE-induced IL-1α production was inhibited by catalase, anti-EGF antibody, PD153035 (EGF receptor antagonist) and U0126 (MEK inhibitor) but not by α-naphthoflavone (cytochrome p450-1A1 inhibitor). ANE-induced ADAM17 production was inhibited by pp2 (Src inhibitor), U0126, α-naphthoflavone and aspirin. AG490 (JAK inhibitor) prevented ANE-stimulated ADAM17, IL-1α, PGE2 production, COX-2 expression, ADAM9 maturation, and the ANE-induced decline in keratin 5 and 14, but showed little effect on cdc2 expression and EGF production. Moreover, ANE-induced 8-isoprostane production by GKs was inhibited by catalase, anti-EGF antibody, AG490, pp2, U0126, α-naphthoflavone, Zinc protoporphyrin (ZnPP) and aspirin. These results indicate that AN components may involve in BQ-induced oral cancer by induction of reactive oxygen species, EGF/EGFR, IL-1α, ADAMs, JAK, Src, MEK/ERK, CYP1A1, and COX signaling pathways, and the aberration of cell cycle and differentiation. Various blockers against ROS, EGF, IL-1α, ADAM, JAK, Src, MEK, CYP1A1, and COX can be used for prevention or treatment of BQ chewing-related diseases.

Arecoline N-oxide: its mutagenicity and possible role as ultimate carcinogen in areca oral carcinogenesis.

Abstract: The areca nut is the most widely consumed psychoactive substance in Taiwan, India, and Southeast Asia. It is considered to be an environmental risk factor for the development of oral submucous fibrosis and cancer. Arecoline, the major alkaloid of areca nut, has been known to cause cytotoxicity and genotoxicity in various systems. However, the active compound accounting for arecoline-induced damage in normal human oral cells is still uncharacterized. The present study was undertaken to identify the active metabolite of arecoline that might induce damage in human oral tissues and cause mutagenicity in Salmonella typhimurium tester strains TA 100 and TA 98. It is interesting to find that the major metabolite of arecoline, arecoline N-oxide, is moderately mutagenic to these Salmonella tester strains. This mutagenicity was potently inhibited by sulfhydryl compounds, namely, glutathione, N-acetylcysteine, and cysteine, whereas methionine is inactive in this inhibition. The mutagenicity of arecoline N-oxide was strongly inhibited by the N-oxide reducing agent titanium trichloride. The possible role of arecoline N-oxide in the induction of oral carcinogenesis by areca nut chewing is discussed.