Regular ArticleRepin-Induced Neurotoxicity in Rodents☆,☆☆
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Cited by (23)
Phytochemical identification, acute and subchronic oral toxicity assessments of hydroalcoholic extract of Acroptilon repens in BALB/c mice: A toxicological and mechanistic study
2022, HeliyonCitation Excerpt :These compounds, as a subcategory of the terpenes, constitute a large group of secondary metabolites that are widely distributed in a variety of plants [25]. Previous studies reported that some sesquiterpenes isolate from A. repens have neurotoxicity in rodents and primary cultures of fetal rat brain cells [17, 27]. The Sesquiterpene Lactones family has been introduced as the most probable cause of toxicity induced by A. repens [15, 28].
Diseases of the Nervous System
2019, Large Animal Internal MedicineToxicology for the Equine Practitioner
2015, Veterinary Clinics of North America - Equine PracticeCitation Excerpt :Two plants in the Asteraceae family are known to cause ENPE: yellow star-thistle (Centaurea solstitialis) and Russian knapweed (Acroptilon repens). Repin, a constituent within the two toxic plants, is thought to be the toxic principle responsible for the development of this disease.2 The exact mechanism by which repin causes ENPE is uncertain.
Extrapyramidal system neurotoxicity. animal models.
2015, Handbook of Clinical NeurologyCitation Excerpt :Recent studies of repin in rodents and cultured PC12 neurons (derived from a rat adrenal pheochromocytoma) suggests that the toxin interferes with striatal dopamine release and glutathione metabolism, and promotes oxidative stress: these mechanisms may be involved in the pathogenesis of the nigropallidal lesions (Robles et al., 1998; Tukov et al., 2004b). Rodents exposed to repin did not develop histologic lesions in either the striatum or substantia nigra (Robles et al., 1998). Toxicant-exposed animals have been used as experimental models for parkinsonism syndromes.
Cytotoxic activity of extracts from Hypochaeris radicata
2013, ToxiconCitation Excerpt :The EC50 (effective concentration producing 50% cytotoxicity (Robles et al., 1997)) for repin in our studies was 3–30 μg/mL (8.2–82 μmol/L) for all 3 cell types. Despite its broad cytotoxicity in vitro, repin, when given intraperitoneally to C57BL/6 mice and Sprague–Dawley rats, was reported to induce a fatal neurologic syndrome associated with increased striatal dopamine levels and a strikingly selective reduction in striatal and hippocampal glutathione (Robles et al., 1998). Cerebral and cerebellar glutathione levels were unaffected.
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Presented in part at the 71st annual meeting of the American Association of Neuropathologists, San Antonio, TX.
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R. F. KeelerK. R. Van KampenL. F. James
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