Cicutoxin

258.361

258.36

Prisms from ether + petroleum ether /(-)-form/; crystals from ether + petroleum ether /(+-)-form/

2905399090

40.5

4.55 (est)

1.025g/cm3

67 °C

467.2ºC at 760mmHg

218.3ºC

1.547

soluble in alcohol, chloroform, ether, hot water, alkali hydroxides; practically insoluble in petroleum ether /(-)-form/

3.34X10-8 mm Hg at 25 deg C (est)

Specific optical rotation: -14.5 deg at 15 °C/D (c= 1.7 in ethanol) /(-)-form/; maximum absorption (alcohol): 242, 252, 318.5, 335.5 nm (e x 10-3= 14.6, 21.6, 50.6, 60.3) /(+-)-form/

Henry's Law constant = 1.41X10-7 atm-cu m/mol at 25 °C (est)

Transformed in light and air to yellow, oily resin|Rapidly decomposes at temperatures above 35 °C|Hydroxyl radical reaction rate constant = 2.66X10-10 cu cm/molec-sec at 25 °C (est)

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

LD50 Mouse ip 48.3 mg/kg

Cicutoxin, a diacetylenic diol, is found in the water hemlock, Cicuta maculata, and other Cicuta spp(1). All parts of the poison-hemlock plant are toxic. The root or tubers of water hemlock are toxic; however, experimental evidence concerning the toxicity of other plant parts is inconclusive(2).

Absorption of cicutoxin is rapid and occurs through the skin as well as through the gut.

... An unsaturated aliphatic alcohol that produces toxicity by central cholinergic stimulation.|... Cicutoxin (a C17-polyene), has been shown to be a potent blocker of potassium channels of T lymphocytes. A similar action on potassium channels of neurons could account for the central nervous system effects.|... Cicutoxin produced a dose-dependent [5 x 10(-6) to 7 x 10(-5) mol/l] and completely reversible block of K+ currents with an EC50 of 1.8 x 10(-5) mol/l. A maximum block of 71% was achieved with cicutoxin at a concentration of 7 x 10(-5) mol/l. ... At noncytotoxic concentrations [10(-7) to 5 x 10(-5) mol/l] cicutoxin reduced the 3H-thymidine incorporation dose-dependently.

Immediate gastric evacuation should be performed by whatever means are available and benzodiazepines should be administered for seizures. In addition, treatments with hemodialysis, anticholinergic therapy, and sodium thiopentone infusion are recommended in separate case reports as potential life-saving measures.|Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ Ingestion of as little as a 2 cm section of the sweet-tasting root of Cicuta can produce fatal status epilepticus; a child's use of a stem as a toy whistle caused the child's death. The cause of seizures is not clear but may be from central cholinergic overstimulation, sodium channel effects, or blockade of potassium dependent channels.|/SIGNS AND SYMPTOMS/ A single tuber /of Cicuta maculata (water hemlock)/ may cause fatal poisoning, characterized by tonic-clonic convulsions.|/SIGNS AND SYMPTOMS/ Symptoms of mild or early poisonings consist of GI symptoms (nausea, vomiting, epigastric discomfort) and begin as early as 15 minutes after ingestion. Emesis may diminish the toxic load in the gut. Diaphoresis, flushing, dizziness, excessive respiratory distress, and cyanosis occur, and rapidly progress to violent seizures that are the probably cause of death. Complications include rhabdomyolysis with renal failure and severe acidemia.|/CASE REPORTS/ Water hemlock (Cicuta maculata) poisoning in a 26-year-old man resulted in rhabdomyolysis and acute renal failure. The epidemiology and clinical features of Cicuta poisoning are discussed.|For more Human Toxicity Excerpts (Complete) data for CICUTOXIN (6 total), please visit the HSDB record page.

Cicutoxin, a diacetylenic diol, is found in the water hemlock, Cicuta maculata, /C. douglasii/ and other Cicuta spp.