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Sodium fluoroacetate is the organofluorine compound with the formula FCH2CO2Na. This colourless salt is used as a metabolic poison. It occurs naturally as an anti-herbivore metabolite in various plants but can also be produced synthetically. It is a derivative of fluoroacetic acid, a carboxylic acid. The more common fluorinated acetic acid trifluoroacetic acid and its derivatives are far less toxic.
[edit] History and productionThe effectiveness of sodium fluoroacetate as a rodenticide was reported in 1942.[1] The name "1080" refers to the catalogue number of the poison, which became its brand name.[2] The salt is synthesized by treating sodium chloroacetate with potassium fluoride.[3] Production has declined because the salt is banned in many countries. [edit] OccurrenceSodium fluoroacetate occurs naturally in at least 40 plants in Australia, Brazil, and Africa. It was first identified in the poison leaf Dichapetalum cymosum by Marais in 1944.[4][5] As early as 1904, colonists in Sierra Leone used extracts of Chailletia toxicaria which also contains fluoroacetic acid or its salts to poison rats.[6][7] It is believed that the compound is even present in tea leaves in tiny amounts.[8] The Australian pea family Gastrolobium (“poison peas”), have sodium fluoroacetate in the leaf tips and seeds. Its occurrence forces livestock farmers in Western Australia to hand-weed their paddocks. [edit] ToxicologyFluoroacetate is highly toxic to mammals and insects.[2] The oral dose of fluoroacetate sufficient to be lethal in humans is 2–10 mg/kg.[9] The toxicity varies with species. The New Zealand Food Safety Authority established lethal doses for a number of species. Dogs, cats and pigs appear to be most susceptible to poisoning.[10] The Fluoroacetate Dehydrogenase enzyme has been discovered in a soil bacterium, which can detoxify fluoroacetate in the surrounding medium. [edit] Mechanism of actionFluoroacetate is similar to acetate, which has a pivotal role in cellular metabolism. Fluoroacetate disrupts the citric acid cycle (also known as the Krebs cycle) by combining with coenzyme A to form fluoroacetyl CoA, which reacts with citrate synthase to produce fluorocitrate. A metabolite of fluorocitrate binds very tightly to aconitase, thereby halting the citric acid cycle. This inhibition results in an accumulation of citrate in the blood which deprives cells of energy.[2] [edit] SymptomsIn humans the symptoms of poisoning normally appear between 30 minutes and three hours after exposure. Initial symptoms typically include nausea, vomiting and abdominal pain; sweating, confusion and agitation follow. In significant poisoning cardiac abnormalities including tachycardia or bradycardia, hypotension and ECG changes develop. Neurological effects include muscle twitching and seizures; Consciousness becomes progressively impaired after a few hours leading to coma. Death is normally due to Ventricular arrhythmias, progressive hypotension unresponsive to treatment, and secondary lung infections.[2] Symptoms in domestic animals vary: dogs tend to show nervous system signs such as convulsions and uncontrollable running, whilst large herbivores such as cattle and sheep more predominantly show cardiac signs.[citation needed] Sub-lethal doses of sodium fluoroacetate may cause damage to tissues with high energy needs — in particular, the brain, gonads, heart, lungs and fetus. Sub-lethal doses are typically completely metabolised and excreted within four days.[citation needed] [edit] TreatmentEffective antidotes are unknown. Research in monkeys has shown that the use of glyceryl monoacetate can prevent problems if given after ingestion of sodium fluoroacetate, and this therapy has been tested in domestic animals with some positive results. In theory, glyceryl monoacetate supplies acetate ions to allow continuation of cellular respiration which the sodium fluoroacetate had disrupted.[citation needed] In clinical cases, use of muscle relaxants, anti-convulsants, mechanical ventilation, and other supportive measures may all be required. Few animals or people have been treated successfully after significant sodium fluoroacetate ingestions. [edit] UsesSee also: 1080 usage in New Zealand Sodium fluoroacetate is used as a pesticide especially for mammalian pest species. Farmers and graziers use the poison to protect pastures and crops from various herbivorous mammals. It is used in New Zealand to control the Common Brushtail Possum and rats.[11] In the United States it is used to kill coyotes. Other countries using 1080 include Australia, Mexico, and Israel.[2] Western Shield is a project to boost populations of endangered mammals in south-west Australia. The project entails distributing fluoroacetate baited meat from the air to kill predators. Wild dogs and foxes will readily eat the baited meat. Cats pose a greater difficulty as cats aren’t interested in already dead animals. Recently a pilot tried putting small sound generators inside the baits with significant positive results.[citation needed] However, an Australian RSPCA commissioned study criticized 1080 calling it an inhumane killer.[12] Some Western Australian herbivores have, by natural selection, developed partial immunity to the effects of fluoroacetate; this aspect has been used for an advantage in DEC’s wildlife conservation project named Western Shield. [edit] Environmental impact
Sodium fluoroacetate slowly decomposes in soil and water in low temperatures, resulting in continued persistence in the environment[13]. Damage to non-target native species occurs and varies depending on the species. In New Zealand the assumption is made that the environmental costs of using sodium fluoroacetate are less than the benefits but research is needed to verify this stance.[14] The video "Poisoning Paradise" illustrates the detrimental environmental effects of sodium fluoroacetate.[1] [edit] References
[edit] Further reading
[edit] External links
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