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When seedlings are in the cotyledonary stage, they are palatable but also have the highest toxicity. Poisoning generally results when these leaves are eaten. This situation occurs most often at the edges of ponds, lakes, floodplains, or other bodies of water where shallow flooding followed by recession of the waterline occurs. Under such conditions seeds germinate readily, constantly supplying new generations of potentially poisonous seedlings as the water source dries out. Animals are attracted to such areas because of their need for drinking water. The problem is accentuated because Xanthium seeds have a natural dormancy and can germinate over long periods of time. Ingestion of cotyledons to 0.75 to 1.5 percent of the animal's body weight will cause toxicity.
Toxicity decreases rapidly as true leaves are formed. Evidence of poisoning appears in about 12 to 48 hours, the symptoms being nausea, vomiting, lassitude, depression, weakened muscles, and prostration. Sever poisoning may result in convulsions and spasmodic running movements. Ruminants may not vomit, but death may occur within a few hours or days. Fatty substances such as milk, lard, or linseed oil have been recommended as antidotes (Kingsbury 1964). The toxic agent in Xanthium may also be responsible for allelopathic effects (Cutler 1983).
J Ethnopharmacol. 2005 Sep 14;100(3):260-7. Links
Anti-ulcerogenic activity of xanthanolide sesquiterpenes from Xanthium cavanillesii in rats.
Favier LS, Maria AO, Wendel GH, Borkowski EJ, Giordano OS, Pelzer L, Tonn CE.
INTEQUI-CONICET-UNSL, Departamento de Quimica, Facultad de Quimica, Bioquimica y Farmacia, Universidad Nacional de San Luis, 5700 San Luis, Argentina.
The preventive effect of natural xanthanolides as well as a series of synthetic derivatives on ulcer formation induced by absolute ethanol in rats was examined. Among the compounds tested, xanthatin gave the strongest protective activity. The inhibitory action exerted by this molecule on the lesions induced by 0.6N HCl and 0.2N NaOH was highly significant, reducing ulceration in the range of 58-96% at a dose from 12.5 to 100mg/kg. These results appear to confirm that the presence of a non-hindered alpha,beta-unsaturated carbonyl group seems to be an essential structural requirement for the gastric cytoprotective activity of these compounds. In order to explore this possibility, a theoretical conformational analysis was performed. We suggest that the mechanism of protection would involve, at least in part, a nucleophylic attack of the sulfhydryl group from the biological molecules present in the gastric mucosa to electrophylic carbons accessible in suitable Michael acceptors.