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Ce produit n'est pas destiné à diagnostiquer, traiter, guérir ou prévenir toute maladie. Ces déclarations n'ont pas été évaluées par la Food and Drug Administration.
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Ces informations sont fournies à titre éducatif uniquement et ne remplacent pas un avis médical professionnel, un diagnostic ou un traitement. Consultez toujours votre professionnel de santé avant d'utiliser des plantes, surtout si vous êtes enceinte, allaitez, prenez des médicaments ou avez une condition médicale.
Prunus dulcis var. amara
Variété du Moyen-Orient d'amande contenant de l'amygdaline; utilisée historiquement pour la toux et comme antispasmodique.
Bitter almond (Prunus dulcis var. amara) is a variety of almond containing the cyanogenic glycoside amygdalin, which upon hydrolysis yields hydrocyanic acid (cyanide), benzaldehyde, and glucose. Historically used in Persian and Middle Eastern traditional medicine as a cough suppressant and antispasmodic, its clinical application is severely limited due to high toxicity. The primary active compounds include amygdalin, benzaldehyde, and emulsin, with cyanide being the principal toxic agent.
Amygdalin is hydrolyzed by the enzyme emulsin (beta-glucosidase) in the gastrointestinal tract to release hydrocyanic acid (HCN). HCN binds to cytochrome c oxidase (Complex IV) in the mitochondrial electron transport chain, inhibiting cellular respiration and causing histotoxic hypoxia. Benzaldehyde contributes to the characteristic bitter almond odor and may have mild antispasmodic effects via modulation of smooth muscle calcium channels, but this is overshadowed by cyanide toxicity. The overall pharmacological effect is dose-dependent respiratory depression and potential for fatal cyanide poisoning.
Variété du Moyen-Orient d'amande contenant de l'amygdaline; utilisée historiquement pour la toux et comme antispasmodique.
Bitter almond (Prunus dulcis var. amara) is a variety of almond containing the cyanogenic glycoside amygdalin, which upon hydrolysis yields hydrocyanic acid (cyanide), benzaldehyde, and glucose. Historically used in Persian and Middle Eastern traditional medicine as a cough suppressant and antispasmodic, its clinical application is severely limited due to high toxicity. The primary active compounds include amygdalin, benzaldehyde, and emulsin, with cyanide being the principal toxic agent.
Amygdalin is hydrolyzed by the enzyme emulsin (beta-glucosidase) in the gastrointestinal tract to release hydrocyanic acid (HCN). HCN binds to cytochrome c oxidase (Complex IV) in the mitochondrial electron transport chain, inhibiting cellular respiration and causing histotoxic hypoxia. Benzaldehyde contributes to the characteristic bitter almond odor and may have mild antispasmodic effects via modulation of smooth muscle calcium channels, but this is overshadowed by cyanide toxicity. The overall pharmacological effect is dose-dependent respiratory depression and potential for fatal cyanide poisoning.