Sodium Monofluoroacetate Poisoning

Trabes, J., Rason, N., Avrahami, E., 1983. Computed tomography demonstration of brain damage due to acute sodium monofluoroacetate poisoning. J. 

Batcheler, C.L. and C.N. Challies. 1988. Loss of compound 1080 (sodium monofluoroacetate) from carbopol gel smeared on foliage to poison deer. N.Z. Jour. Forest. Sci. 18 109-115. 

Savarie, P.J., G.H. Matschke, R.M. Engeman, and K.A. Fagerstone. 1994. Susceptibility of prairie dogs to compound 1080 (sodium monofluoroacetate) baits and secondary poisoning effects in European ferrets under laboratory conditions. Pages 134-143 in A.A. Seawright and C.T. Eason (eds.). Proceedings of the Science Workshop on 1080. Roy. Soc. N.Z., Misc. Ser. 28. 

Spurr, E.B. 1991. Reduction of wasp (Hymenoptera Vespidae) populations by poison-baiting experimental use of sodium monofluoroacetate (1080) in canned sardine. N.Z. Jour. Zool. 18 215-222. 

Of special interest are secondary intoxications due to free-ranging birds consuming carrions of animals that died of rodenticide poisoning. Strychnine and sodium monofluoroacetate are other rodent control compounds that are involved because they cause acute death in the primary victims and are thus present in high concentrations in carrions. 

Strychnine-poisoned birds show clinical effects within 2h of ingesting the product. The birds become apprehensive and nervous and have violent tetanic convulsions, which cause them to become exhausted and to die of hypoxia. Sodium monofluoroacetate causes overstimulation of the CNS and myocardial depression. Cardiac failure is the cause of death and occurs within 1 h of consuming the product or contaminated carcass. 

Fluoroacetate, also known as compound 1080, sodium monofluoroacetate (SMFA), and sodium fluoroacetate, is one of the most toxic substances known. In the past. It was used primarily as a rodenticide by licensed pest control companies, but It has been removed from the US market because of its hazard. (However, it is still used as packets attached to sheep to poison wolves and coyotes that kill and ingest the sheep.) It is a tasteless, odorless, water-soluble white crystalline powder. Fluoroac-etamide (compound 1081) is a similar compound with similar toxicity. 

Brockmann, J.L., McDowell, A.V., Leeds, W.G., 1955. Fatal poisoning with sodium monofluoroacetate. Report of case. J. Am. Med. Assoc. 59,1529-1532. Buffa, P., Pasquali-Ronchetti, J., 1977. Biochemical lesions of respiratory enzymes and configurational changes of mitochondria in vivo. II. Early ultrastructural modifications correlated to the biochemical lesion induced by fluoroacetate. Cell Tissue Res. 183, 1-23. 

Among the most deadly of simple compounds is sodium fluoroacetate. The LD50 (the dose lethal for 50% of animals receiving it) is only 0.2 mg/kg for rats, over tenfold less than that of the nerve poison diisopropylphosphofluoridate (Chapter 12).a b Popular, but controversial, as the rodent poison "1080," fluoroacetate is also found in the leaves of several poisonous plants in Africa, Australia, and South America. Surprisingly, difluoroacetate HCF2-COO is nontoxic and biochemical studies reveal that monofluoroacetate has no toxic effect on cells until it is converted metabolically in a "lethal synthesis" to 2R,3R-2-fluorocitrate, which is a competitive inhibitor of aconitase (aconitate hydratase, Eq. 13-17).b This fact was difficult to understand since citrate formed by the reaction of fluorooxalo-acetate and acetyl-CoA has only weak inhibitory activity toward the same enzyme. Yet, it is the fluorocitrate formed from fluorooxaloacetate that contains a fluorine atom at a site that is attacked by aconitase in the citric acid cycle. 

Fluoroacetate (3), the sodium salt of monofluoroacetic acid, is also a substance of vegetable origin, reported to poison sheep and cattle repeatedly. It is the toxic substance of a South African plant called gifblaar (Dichapetalum cymostm) and of the Australian plant Acacia georginae (Marais, 1944). The compound is readily soluble in water and is very toxic. Its acute oral lDj for rats is 0.2-2 mg/kg. The compound is converted via the citrate cycle into fluorocitrate and this blocks the citrate cycle. 

---