China 
Africa 
Explore chapters and articles related to this topic
Asymmetric Reduction of C=N Bonds by Imine Reductases and Reductive Aminases
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Matthias Höhne, Philipp Matzel, Martin Gand
The amino acid sequences are known for most of these enzymes. An exception is γ-coniceine reductase, the IRED catalyzing the last step in coniine biosynthesis (Table 14.1, entry 6) (Hotti and Rischer, 2017). This is the toxic alkaloid produced in the plant poison hemlock (Conium maculatum), which killed Sokrates.
H
Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Hemlock (Conium maculatum) Mentioned in Greek literature dating back to 400 BC. Medicinal effects were known to the ancients and Dioscorides (AD 40–90) recommended it in his De Materia Medica as a soothing ointment. The famous hemlock potion by which Greek criminals were put to death was essentially composed of the juice. The effects of hemlock as a poison in the official execution of Socrates (c 469–399 BC), were described by Plato (428–347 BC) in Phaedo: ‘Socrates after swallowing the poison cup walked about for a short time as he was directed by the executioner; when he felt a sense of heaviness in his limbs he laid down on his back; his feet and legs fast lost their sensibility and became stiff and cold; and the state gradually extended towards the heart, when he died convulsed’. The effect was also described by Nicander in 100 BC who advocated undiluted wine as a remedy for poisoning by the plant. The Abbess Hildegard in the 12th century recommended it for treatment of swellings, and it remained in the pharmacopoeia for centuries. Johannes Storch (1681–1751) was responsible for popularizing its use in medicine as a narcotic. The poisonous nature of the plant was found to be due to the alkaloids, coniine, methyl coniine, conicene and conhydrine. Giescke isolated coniine in 1827, it was incidentally the first alkaloid to be synthesized.
Catalog of Herbs
Published in James A. Duke, Handbook of Medicinal Herbs, 2018
Toxicity — Classed appropriately by the FDA as an unsafe herb62 containing the poisonous alkaloid coniine, and other closely related alkaloids. Plant can also cause contact dermatitis. Ingestion may cause debility, drowsiness, nausea, labored respiration, paralysis, asphyxia, and death.20 Following lethal doses, animals rapidly begin to show symptoms; among them: paralysis of the tongue, mydriasis, head pressure, giddiness, nausea, vomiting, diarrhea, and collapse into central paralysis, first the feet and legs, then the buttocks, arms, then paralysis of the swallowing and speech. With increasing dyspnea and cyanosis, death ensues through central respiratory paralysis. Lethal dose is about 500 to 100 mg coniine for man.33
Mistaken identity: acute respiratory arrest from accidental ingestion of poison hemlock
Published in Clinical Toxicology, 2022
Kai Li, Hillary Bassett, Briana Fitch, Kara Lynch
Poison Hemlock (Conium maculatum) is a commonly occurring member of the parsley family and misidentification of the plant may lead to accidental ingestion. The stem is characteristically hollow with purple-red splotches [1] (Figure 1). Toxicity occurs as a result of its eight nicotinic alkaloids, the most potent being coniine. These alkaloids are selective nicotinic-type acetylcholine receptor (nAChRs) agonists that have effects on both the autonomic and skeletal muscles. Initial symptoms include nausea, vomiting, salivation, bronchorrhea, tachycardia, hypertension, agitation, confusion, and muscle fasciculations. With a higher dose, the nicotinic alkaloids can cause a delayed phase of toxicity characterized by a paradoxical blockage of the nicotinic receptors. This results in bradycardia, hypotension, muscle paralysis, lethargy, and respiratory muscle paralysis [2].
Disposition of toxic drugs and chemicals in man
Published in Clinical Toxicology, 2021
Other changes have made the new edition as indispensable as its predecessors. The first of these is the enlargement of the scope to include some important and well-established natural poisons. These include, for example, brief accounts of aristolochic acid, the cause of renal failure in a cohort of Belgian women attempting to lose weight; coniine, the instrument of Sophocles’s execution; and domoic acid, the excitatory amino acid responsible for neurotoxic shellfish poisoning. There are also, inevitably, new drugs of abuse, such as 2-fluorofentanyl, 3-methoxyphencyclidine, and mexedrone. Dipropyltryptamine, flualprazolam, and the phenethylamine derivative 25H-NBOMe are among the 19 compounds of emerging interest that squeeze into the Addendum, complete with references to the recent literature. In total, more than 280 new entries appear in this edition. The whole range spans the alphabet from abacavir to zuclopenthixol.