Catalog of Herbs
James A. Duke in Handbook of Medicinal Herbs, 2018
Nuts contain the alkaloids, arecoline, arecaine, arecaidine, and arecolidine, isoguvacine, guvacine, and guvacoline; tannins (18%), (tannic- and gallic-acid), fats (14 to 18%; with glycerides of palmitic-, stearic-, myristic-, lauric-, oleie-, margaric-, nonadecanoid-, and heneicosanic-acids), choline, catechin, saccharose, mannan, galactan, other carbohydrates and proteins, and some Vitamin A.1 Gum, mucilage, and resin are also reported. Per 100 g, the shoot is reported to contain 43 calories, 86.4 g H2O, 3.3 g protein, 0.3 g fat, 9.0 g total carbohydrate, 1.0 g ash, 6 mg Ca, 89 mg P, and 2.0 mg Fe. Per 100 g, the mature seed is reported to contain 394 calories, 12.3 g H2O, 6.0 g protein, 10.8 g fat, 69.4 g total carbohydrate, 15.9 g fiber, 1.5 g ash, 542 mg Ca, 63 mg P, 5.7 mg Fe, 76 mg Na, 446 mg K, 0.17 mg thiamine, 0.69 mg riboflavin, 0.6 mg niacin, and a trace of ascorbic acid.21
Abies Spectabilis (D. Don) G. Don (Syn. A. Webbiana Lindl.) Family: Coniferae
L.D. Kapoor in Handbook of Ayurvedic Medicinal Plants, 2017
Chemical constituents — Ripe and semiripe areca nuts contain26 a large number of amino acids both in the free and combined state. The salient features of amino acid makeup are an insignificant quantity of tryptophan and methionin, presence of high percentage of proline both in free and combined forms, and relative increase of free tryosine and phenylalanine and of combined arginine in the semiripe and ripe nuts. Earlier investigations revealed the presence of five alkaloids, viz., arecoline, arecaidine, guvaoline, guvacine, and arecolidine, but a recently detailed analysis of young and mature nuts showed the presence of minor amounts of + catechin and high amounts of procyanidins.105 Arecoline, a substitute for pilocarpine, has been isolated from the nuts. They also contain β-sitosterol and leukocyanidins and tannins which exhibit antibacterial and antifungal properties.178
Parasympathomimetic Amines
Kenneth J. Broadley in Autonomic Pharmacology, 2017
Arecoline has been the basis for many newer synthetic muscarinic agonists since it has a rigid structure with little opportunity for conformational flexibility at the muscarinic receptor binding sites. In general, muscarinic agonists do not tolerate addition of steric bulk. With arecoline, addition of a methyl group at the 4-position or lengthening of the side-chain to an O-n-propyl group converts it to antagonist molecules (Table 8.2). This lack of tolerance may be due to the fact that agonist binding to aspartate residues (eg Asp-147) within the seven membrane-spanning domains of the muscarinic receptor is fairly precise. Differences in amino acid sequence and topography between receptor types is also very limited so that agonist selectivity is difficult to obtain. An exception to this rule with increasing size of substitution is the introduction of bulky side-chains with a propargyl moiety. Such a group was present in the first M1 selective agonist, McN-A-343. Addition of propargyl-containing side-chains to arecoline has generated several analogues of which arecaidine propargyl ester (APE) is a potent agonist with three-fold functional selectivity for M2 receptor-mediated atrial negative inotropic responses compared with the ileum (M3). It also has potent M1 agonist activity, like McN-A-343, and increases heart rate in the pithed rat (Moser et al. 1989). Aceclidine is a synthetic muscarinic agonist resembling arecoline which was first used over 20 years ago to reduce intraocular pressure in glaucoma with equal effectiveness to pilocarpine.
Metabolism of the areca alkaloids – toxic and psychoactive constituents of the areca (betel) nut
Published in Drug Metabolism Reviews, 2022
Alan L. Myers
An unanticipated major in vivo metabolite of arecoline and arecaidine is N-methylnipecotic acid, a derivative lacking a double bond in the piperidinyl ring and containing a de novo chiral carbon with unknown stereochemistry. In regards to xenobiotic metabolism, this type of reduction is uncommon and it is not surprising that the enzyme(s) and tissue site(s) facilitating the reaction remain unknown. Giri et al. (2006), probably the first to identify this metabolite in vivo, postulated that N-methylnipecotic acid is formed from an acyl-CoA ester of arecaidine and a putative catalyst is trans-2-enoyl thioester reductase (Giri et al. 2006). Another possibility, in the author’s opinion, is the bacterial NADH-dependent morphinone reductase that reduces codeinone and morphinone to hydrocodone and hydromorphone, respectively (French and Bruce 1994). Morphinone reductase belongs to a class of oxidoreductases that are similar to the old yellow enzyme (OYE) family (Messiha et al. 2005). Messiha et al. (2005) showed that morphinone reductase metabolizes α/β unsaturated carbonyl compounds such cyclohexen-1-one (Messiha et al. 2005). The arecoline molecule, interestingly, contains an α/β unsaturated carbonyl system. Confirmation of enzymes driving stereospecific N-methylnipecotic acid formation is unknown, but possibly toxicologically relevant since removal of the double bond presumably abolishes the reactivity of arecoline with important cellular thiols. Thus, formation of N-methylnipecotic acid stereoisomers is a potential detoxification marker, clearly justifying further research.
Text, picture or video: effects of different consumption guidance methods on betel nut sensory evaluation and risk perception
Published in Journal of Substance Use, 2022
Hong Wen, Hong Zheng, Lifang Li, Fengshan Li
Betel nut (BN) is the fourth most popular psychoactive substance in the world (IARC, 2004). The arecoline and arecaidine in BN can increase the adrenaline, resist anxiety, and make people excited and addicted (Chu, 2001; Lim, 2003). Meanwhile, BN has been listed as a first-class carcinogen by the World Health Organization (IARC, 2004). It is confirmed that BN has certain damage on the body’s energy metabolism regulation and immune response, such as hyperglycemia, atherosclerosis, and inflammation (Wei et al., 2017). Chewing BN will also cause great damage to the oral cavity (Chang et al., 2017), including oral ulcers, oral mucosa damage, and even oral leukoplakia and oral submucous fibrosis, which are high-risk preneoplastic states (Lee et al., 2003).