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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.
Aristolochia clematitis
La cataire européenne était historiquement utilisée pour l'accouchement et les blessures; interdite dans l'UE en raison de sa néphrotoxicité.
Aristolochia clematitis, commonly known as European birthwort, is a herbaceous plant historically used in traditional medicine for inducing childbirth and treating wounds. However, it contains aristolochic acids I and II, which are potent nephrotoxins and carcinogens, leading to its ban in many countries. Modern evidence confirms severe renal toxicity and mutagenicity, with no safe internal use.
Aristolochic acids (AAs) are metabolically activated by nitroreduction to form DNA adducts, primarily at adenine residues, leading to mutations in the TP53 tumor suppressor gene and activation of oncogenes. These adducts also cause proximal tubular cell necrosis and progressive interstitial fibrosis via mitochondrial dysfunction and oxidative stress. The resulting aristolochic acid nephropathy (AAN) is characterized by rapid renal failure and a high risk of urothelial carcinoma. Additionally, AAs inhibit CYP1A2 and CYP3A4, potentially altering drug metabolism.
La cataire européenne était historiquement utilisée pour l'accouchement et les blessures; interdite dans l'UE en raison de sa néphrotoxicité.
Aristolochia clematitis, commonly known as European birthwort, is a herbaceous plant historically used in traditional medicine for inducing childbirth and treating wounds. However, it contains aristolochic acids I and II, which are potent nephrotoxins and carcinogens, leading to its ban in many countries. Modern evidence confirms severe renal toxicity and mutagenicity, with no safe internal use.
Aristolochic acids (AAs) are metabolically activated by nitroreduction to form DNA adducts, primarily at adenine residues, leading to mutations in the TP53 tumor suppressor gene and activation of oncogenes. These adducts also cause proximal tubular cell necrosis and progressive interstitial fibrosis via mitochondrial dysfunction and oxidative stress. The resulting aristolochic acid nephropathy (AAN) is characterized by rapid renal failure and a high risk of urothelial carcinoma. Additionally, AAs inhibit CYP1A2 and CYP3A4, potentially altering drug metabolism.