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Convulsions plant

Twenty-two cases of endosulfan poisoning were reported in people exposed while spraying cotton and rice fields the dermal route of exposure was assumed to be the primary route of exposure (Singh et al. 1992). The assumption was based on the fact that those spraying rice fields, and who suffered cuts over the legs with the sharp leaves on the rice plants exhibited the more severe toxicity. Three out of the 22 cases exhibited tremors and 11 presented convulsions all patients recovered. [Pg.119]

Risa J, Risa A, Adsersen A, et al. Screening of plants used in southern Africa for epilepsy and convulsions in the GABAA-benzodiazepine receptor assay. J Ethnophar-macol 2004 93 177-182. [Pg.166]

Physiological Action.—Vanadium compounds are poisonous when taken internally.1 The usual symptoms are paralysis, convulsions, lowering of the body temperature, and feeble pulse. The fatal dose in the case of a rabbit is between 0-00918 and 0-01466 gram. Workmen exposed to fumes of vanadium compounds, especially those engaged on ore-reduction plants, are said to be susceptible to vanadium poisoning, but this has been denied.2 Vanadium compounds have been shown... [Pg.22]

Specific antagonists for GABAa receptors include the alkaloid convulsants bicuculline (Fig. 30-25)699 and picrotoxin (Fig. 22-4) and the convulsant terpenoid compound thujone (Fig. 22-3), which is present in the wormwood plant Artemesia absinthium. Thujone is present in the liqueur absinthe, which was the national drink of France in the late 19th century but, because of its toxicity, has been illegal in most countries since -1915.719... [Pg.1789]

Ingestion of copper sulfate by humans causes vomiting, cramps, convulsions, and as little as 27 grams of the compound may cause deulh. An important part of the toxicity of copper to both plants and animals is probably due to its combination with thiol groups of certain enzymes, thereby inactivating them. The effects ol chronic exposure to copper in animals are cirrhosis of the liver, failure of growth, and jaundice. [Pg.442]

A deficiency of the vitamin can result in lymphopenia, convulsions, dermatitis, irritability, and nervous disorders in humans. A defidency in monkeys may cause arteriosclerosis, while in rats, acrodynia. Research indicates that all animals require vitamin Bg, Bacteria in intestines generate some of this vitamin, but relatively little is available to humans in this form. Endogenous sources are available to plants, fungi, and some bacteria. [Pg.1701]

It is a toxic plant and has properties similar to strychnine, which is obtained from Strychnos nux vomica. Once recommended as a remedy for cholera, the plant is used to treat fever and acute emotional and mental afflictions such as hysteria, insomnia, and depression. In toxic doses, it causes muscle spasms, painful convulsions, and even death by asphyxiation (see Chapter 62). [Pg.134]

This toxic protein is contained in caster seeds but does not pass into the oil. Similar phytotoxins occur in croton seeds (Crotin) jequirity seeds (Abrin) the bark of the locust tree, Robinia pseudo-acacia (Robin) and in the seeds of some leguminous plants (Phasin). The last is but weakly toxic. Ricin is responsible for the toxic effects on eating castor seeds 5 or 6 of these are fatal to a child, 20 to adults, and 3 or 4 seeds may cause violent gastroenteritis with nausea, headache, persistent vomiting, colic, sometimes bloody diarrhea, thirst, emaciation, and great debility. The symptoms usually do not set in until after several days. More severe intoxications cause small frequent pulse, cold sweat, icterus, and convulsions. Death occurs in 6 to 8 d, from the convulsions or from exhaustion. The fatality rate is about 6%. This low fatality rate is due to the destruction of the poison in the alimentary canal. The treatment would be evacuant and symptomatic. Usually, 3 to 10 d are required to complete recovery. [Pg.161]

Sir William Brooke O Shaughnessy introduced Indian hemp to the West in 1839. William Brooke O Shaughnessy entered the service of the East India Company in 1833 as assistant surgeon. He studied the botany and chemistry of herbs used in oriental medicine and incorporated some into his edition of the Bengal Pharmacopoeia published in 1842. One of these herbs was cannabis, or Indian hemp. His medical treatise recommended an extract from the plant for patients with rabies, cholera, tetanus, and infantile convulsions. Until the end of the 19th century prominent physicians of Europe and North America advocated cannabis extracts for the prevention and symptomatic treatment of migraine headache. [Pg.234]


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