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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.
Senecio vulgaris
Common European weed; highly hepatotoxic pyrrolizidine alkaloids; no safe medicinal use.
Senecio vulgaris (common groundsel) is a widespread European weed containing hepatotoxic pyrrolizidine alkaloids (PAs) such as senecionine, seneciphylline, retrorsine, and integerrimine. Despite historical folk use as an emmenagogue and vulnerary, it has no safe medicinal application due to its potential to cause fatal hepatic veno-occlusive disease (HVOD). All internal use is contraindicated, and even topical application carries absorption risks.
Pyrrolizidine alkaloids undergo hepatic CYP450-mediated bioactivation to reactive pyrrolic metabolites that form DNA and protein adducts, leading to sinusoidal endothelial cell injury and obstruction. This triggers glutathione depletion, oxidative stress, and apoptosis, culminating in veno-occlusive disease (sinusoidal obstruction syndrome). The alkaloids also inhibit CYP3A4 and other enzymes, impairing detoxification and increasing susceptibility to hepatotoxicity.
Common European weed; highly hepatotoxic pyrrolizidine alkaloids; no safe medicinal use.
Senecio vulgaris (common groundsel) is a widespread European weed containing hepatotoxic pyrrolizidine alkaloids (PAs) such as senecionine, seneciphylline, retrorsine, and integerrimine. Despite historical folk use as an emmenagogue and vulnerary, it has no safe medicinal application due to its potential to cause fatal hepatic veno-occlusive disease (HVOD). All internal use is contraindicated, and even topical application carries absorption risks.
Pyrrolizidine alkaloids undergo hepatic CYP450-mediated bioactivation to reactive pyrrolic metabolites that form DNA and protein adducts, leading to sinusoidal endothelial cell injury and obstruction. This triggers glutathione depletion, oxidative stress, and apoptosis, culminating in veno-occlusive disease (sinusoidal obstruction syndrome). The alkaloids also inhibit CYP3A4 and other enzymes, impairing detoxification and increasing susceptibility to hepatotoxicity.