Showing papers on "Arecoline published in 1994"

Genotoxic and Non-genotoxic Effects of Betel Quid Ingredients on Oral Mucosal Fibroblasts in vitro:

Abstract: To understand the role of betel quid (BQ) in the pathogenesis of oral submucous fibrosis (OSF) and oral cancer, we used DNA damage, cytotoxicity, and cell proliferation assays to study the pathobiological effects of aqueous extracts of three BQ constituents [betel nut (Areca catechu, BN), inflorescence of Piper betle (IPB), and lime], one BN alkaloid (arecoline), and one BN polyphenol [(+)-catechin] on cultured oral mucosal fibroblasts. Extracts of BN and IPB induced DNA strand break formation in a dose-dependent manner. Extracts of BN and IPB, (+)-catechin, and arecoline decreased cell survival and proliferation in a dose-dependent manner. However, aqueous extract of lime (50-800 micrograms/mL) increased cell proliferation by 20-40%. These results indicate that BQ contains not only genotoxic and cytotoxic agents, but also compounds which stimulate cell proliferation. These compounds may act synergistically in the pathogenesis of OSF and oral cancer in BQ chewers. In addition, five anti-oxidants [glutathione (GSH), cysteine, mannitol, catalase, and superoxide dismutase (SOD)] were tested for their protective effects against the cytotoxicity of BQ constituents. GSH (1.95 and 2.6 mmol/L) and cysteine (4 and 8 mmol/L) prevented the arecoline-induced cytotoxicity. In contrast, mannitol, catalase, and SOD did not decrease the arecoline-induced cytotoxicity. These results indicate that thiol depletion, but not the attack of oxygen free radicals, could be the mechanism for arecoline cytotoxicity. GSH could also protect cells from the cytotoxicity of IPB extract. Increasing dietary intake of GSH-rich foods or dietary supplements of GSH may have chemopreventive potential to reduce BQ-associated oral lesions.

Observations on the effect of areca nut extracts on oral fibroblast proliferation

Abstract: The effects of aqueous extracts of raw, baked and boiled areca nuts were tested on cultured human buccal mucosa fibroblasts. Cells were exposed to extract concentrations of 0, 50, 100, 150, 300 and 500 micrograms/ml. The arecoline and arecaidine content was determined in the extracts with HPLC and raw nut contained 5.5% m/m, baked nut 6.6% m/m and boiled nut 7.1% m/m. Extract concentrations of 50 to 150 micrograms/ml inhibited cell growth in a concentration-dependent manner but did not lead to total cell death during a 7 day period. However, total cell death did occur with concentrations of 300 and 500 micrograms/ml. It is concluded that areca nut extract is toxic to cultured fibroblasts and inhibits their proliferation in a concentration-dependent manner.

Cholinergic REM induction test with arecoline in depressed children

Abstract: Children with major depressive disorder often fail to exhibit electroencephalographic (EEG) sleep abnormalities similar to those reported in depressed adults. It was hypothesized that a cholinergic rapid eye movement (REM) induction test would contribute to the identification of EEG sleep abnormalities in depressed children. To test this hypothesis, prepubertal children meeting research diagnostic criteria for major depressive disorder ( n = 33) and carefully screened healthy control children ( n = 15) were enrolled in a4-day psychobiologic protocol that included 1 night with infusion of arecoline (0.5 mg) during the first non-REM sleep period. Although there had been no significant group differences in baseline sleep measures, results on the arecoline night revealed significantly shorter REM latency in the group of depressed children compared with the control children (mean ± SD=105 ± 51 minutes vs. 140 46 ± minutes). The design of the protocol (with an interval break immediately preceding the arecoline night) prevented a direct estimation of arecoline effects within subjects; however, these data provide promising preliminary results regarding cholinergic REM induction tests in childhood depression.

Short communication two distinct receptors are activated by arecoline on cockroach sixth abdominal ganglion dum neurones

Abstract: During the last decade, extensive biochemical and electrophysiological studies have been performed to characterize the pharmacological properties of cholinergic receptors of insect neurone somata (Sattelle, 1985; Breer and Sattelle, 1987; Benson, 1992). Although most of these studies have been focused on the pharmacological characterization of the cell body nicotinic receptors (Lane et al. 1982; Harrow and Sattelle, 1983; David and Sattelle, 1984; Benson, 1992), evidence for a population of acetylcholine (ACh) receptors exhibiting muscarinic and ‘mixed’ (nicotinic/muscarinic) properties has been reported on insect neurone somata (Benson and Neumann, 1987; Knipper and Breer, 1988; Benson, 1989, 1992, 1993; Trimmer and Weeks, 1989; David and Pitman, 1990, 1992, 1993). One group of insect neurones, called dorsal unpaired median (DUM) neurones, expresses functional cholinergic receptors that differ from the classic vertebrate ACh receptors in that, although DUM neurones were sensitive to ACh, the nicotinic and/or muscarinic nature of these receptors has not been resolved since the cholinergic antagonists abungarotoxin and atropine were relatively ineffective in blocking the ACh response (Goodman and Spitzer, 1980; Lane et al. 1982; Lapied et al. 1990). However, using a range of cholinergic antagonists known to be selective for vertebrate ACh receptors, it has recently been possible to demonstrate the diversity of functional ACh receptors; these include nicotinic, ‘mixed’ and muscarinic receptors mediating specific responses elicited by different cholinergic agonists, such as nicotine, muscarine, oxotremorine and McN-A343, on both isolated and in situ DUM neurones (Lapied et al. 1990, 1992; Bai et al. 1992). Extending these studies, we report in this paper that another cholinergic ligand, arecoline, which is known to act preferentially as a muscarinic agonist in vertebrate preparations (Wess et al. 1990), induced a complex response mediated by both nicotinic and muscarinic receptors on DUM neurones. All experiments were performed on in situ DUM neurones situated along the dorsal midline of the sixth abdominal (A6) ganglion of the nerve cord of adult male cockroaches Periplaneta americana L., obtained from our laboratory stock colony maintained at

Antagonism of diazepam's anticonflict effects in rats by nicotine, but not by arecoline

Abstract: The purpose of the present study was to determine the possible role of cholinergic mechanisms in the anticonflict effects of the anxiolytic diazepam. Male Sprague-Dawley rats were tested with a modified Geller-Seifter procedure using a multiple reinforcement schedule in which unpunished responding in one component was reinforced according to a fixed-interval 60-sec schedule, and punished responding in the other component resulted in both food and a brief electric shock presentation according to a fixed-ratio 1 schedule. In Experiment 1 (−)-nicotine antagonized the increase in punished responding that was produced by diazepam. In Experiment 2 diazepam produced selective increases in punished responding that again was antagonized by (−)-nicotine, a nicotinic cholinergic agonist, whereas arecoline, a muscarinic cholinergic agonist, did not antagonize diazepam's increase in punished responding. Neither drug produced any significant changes in unpunished responding. In Experiment 3 it was shown that the centrally acting nicotinic antagonist, mecamylamine, was able to block nicotine's antagonism of diazepam. These results suggest that there is an interaction between central nicotinic cholinergic mechanisms and diazepam's anticonflict effects in this animal model for anxiolytics, and support clinical observations that smoking can reduce some effects of benzodiazepines. © 1994 Wiley-Liss, Inc.

Bridged 1,2,5,6‐Tetrahydropyridine Esters and Oxime Ethers Related to Arecoline are Novel and Potent Muscarinic Agonists.

Abstract: Constraining the 1,2,5,6-tetrahydropyridine ring of arecoline 1a and the related muscarinic agonists 1b–e by replacing the N-methyl group by an ethano bridge between the nitrogen and the C5-position afforded compounds 2a–e . These compounds have enhanced affinities for muscarinic receptors which supports our proposed binding conformation ( 1a ) ax of arecoline.