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2009
DOI: 10.1080/15563650903252186
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Nicotinic plant poisoning

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Cited by 104 publications
(78 citation statements)
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“…The onset of symptoms in an acute nicotine alkaloid poisoning is usually rapid, within 15-30 min of ingestion and the symptoms often follow a biphasic pattern with initial vomiting and adrenergic stimulation followed by symptoms of ganglionic and neuromuscular blockage [22,23]. The present case is consistent with this pattern of nicotinic intoxication with vomiting and dizziness developing 30 min after ingestion, followed by a respiratory arrest after about 90 min.…”
Section: Discussionsupporting
confidence: 74%
See 1 more Smart Citation
“…The onset of symptoms in an acute nicotine alkaloid poisoning is usually rapid, within 15-30 min of ingestion and the symptoms often follow a biphasic pattern with initial vomiting and adrenergic stimulation followed by symptoms of ganglionic and neuromuscular blockage [22,23]. The present case is consistent with this pattern of nicotinic intoxication with vomiting and dizziness developing 30 min after ingestion, followed by a respiratory arrest after about 90 min.…”
Section: Discussionsupporting
confidence: 74%
“…Poisoning by anabasine is characterized by nicotine-like toxicity. The clinical effects of nicotine alkaloid toxicity are the result of the summation of actions at ganglionic sites, motor end plates, and smooth muscle [17,18,[21][22][23]. Nicotine alkaloids initially stimulate the ganglia of the sympathetic and parasympathetic nervous systems by direct cholinomimetic action on the ganglia.…”
Section: Discussionmentioning
confidence: 99%
“…High levels of anabasine, a piperidine alkaloid isomer of nicotine, have been reported in this plant as far as 1935 (Smith, 1935;Galiana and VigueraLoko, 1964), and confirmed in many other chemical studies (Lisko et al, 2013). Ingestion of this alkaloid can result in severe or lethal poisoning in humans, livestock and poultries (Papavisiliu and Heliakis, 1947;Castorena et al, 1987;Sims et al, 1999;Mizrachi et al, 2000;Schep et al, 2009;Botha et al, 2011;Semmler et al, 2012). Also, teratogenic activity has been attributed to this alkaloid (Keeler et al, 1981;Green et al, 2012).…”
Section: Introductionmentioning
confidence: 99%
“…Nicotine is metabolized in the liver, primarily by cytochrome P450 2A6, generating cotinine, which is probably inactive. The half-life of nicotine averages 2 h, while the half-life of cotinine averages 16 h. Owing to the short half-life of nicotine, cotinine is widely used as a quantitative marker for exposure to nicotine (for example, as a diagnostic test for the use of tobacco) [8,9]. Nicotine acts as an agonist at nicotinic acetylcholine receptors.…”
Section: Discussionmentioning
confidence: 99%