Treatment of 1080 poisoning in dogs with glycerol monoacetate

Rammell, C. G.; Hoogenboom, J.J.L.; Julian, A. F.; Livingstone, Paul G

doi:10.1080/00480169.1985.35203

Cited by 7 publications

(6 citation statements)

References 2 publications

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“…Moreover, these compounds can increase citrate concentration in various organs (Egyed and Shlosberg, 1973). For these reasons, monoacetin and acetamide cannot be recommended for humans (Rammel et al, 1985;Egyed and Schultz, 1986;Spoerke et al, 1986). Cortisol acetate offers certain advantages, since, apart from the primary effect (inhibition of FC synthesis), it prevents ketosis.…”

Section: Therapy For Fa Intoxicationmentioning

confidence: 95%

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Toxicology of fluoroacetate: a review, with possible directions for therapy research

2006

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Fluoroacetate (FA; CH2FCOOR) is highly toxic towards humans and other mammals through inhibition of the enzyme aconitase in the tricarboxylic acid cycle, caused by 'lethal synthesis' of an isomer of fluorocitrate (FC). FA is found in a range of plant species and their ingestion can cause the death of ruminant animals. Some fluorinated compounds -- used as anticancer agents, narcotic analgesics, pesticides or industrial chemicals -- metabolize to FA as intermediate products. The chemical characteristics of FA and the clinical signs of intoxication warrant the re-evaluation of the toxic danger of FA and renewed efforts in the search for effective therapeutic means. Antidotal therapy for FA intoxication has been aimed at preventing fluorocitrate synthesis and aconitase blockade in mitochondria, and at providing citrate outflow from this organelle. Despite a greatly improved understanding of the biochemical mechanism of FA toxicity, ethanol, if taken immediately after the poisoning, has been the most acceptable antidote for the past six decades. This review deals with the clinical signs and physiological and biochemical mechanisms of FA intoxication to provide an explanation of why, even after decades of investigation, has no effective therapy to FA intoxication been elaborated. An apparent lack of integrated toxicological studies is viewed as a limiter of progress in this regard. Two principal ways of developing effective therapies for FA intoxication are considered. Firstly, competitive inhibition of FA interaction with CoA and of FC interaction with aconitase. Secondly, channeling the alternative metabolic pathways by orienting the fate of citrate via cytosolic aconitase, and by maintaining the flux of reducing equivalents into the TCA cycle via glutamate dehydrogenase.

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Section: Therapy For Fa Intoxicationmentioning

confidence: 95%

“…It was established that for successful therapy more than 100 mg kg −1 of monoacetin is required (Engel et al, 1954;Rammel et al, 1985). Monoacetin functions to decrease the level of ketone bodies.…”

Section: Therapy For Fa Intoxicationmentioning

confidence: 99%

Toxicology of fluoroacetate: a review, with possible directions for therapy research

2006

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“…7 Various techniques such as induction of emesis, gastric and peritoneal lavage, and administration of adsorbents, including activated charcoal, colestipol, and anion-exchange resins, have been recommended after 1080 ingestion, 7-10 however limited controlled data exists on their efficacy. A variety of potential antidotes has also been investigated, primarily in rats and mice, including glycerol monoacetate, [11][12][13] actetamide, 14 calcium salts (alone [15][16][17] and in combination with sodium α-ketoglutarate and sodium succinate 18 ), sodium bicarbonate, 19 neurotransmitter modulating agents, [8][9][10]20 and 4-methyl pyrazole. 21 Unfortunately, no single therapy has proven to be an effective treatment for 1080 toxicosis in the dog.…”

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confidence: 99%

Sodium monofluoroacetate (Compound 1080) poisoning in dogs

et al. 2005

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Sodium monofluoroacetate (Compound 1080) is a widely used pesticide for control of feral animals such as the fox. Accidental poisoning of domestic animals occurs despite strict regulations on 1080 usage. Dogs are particularly susceptible to the toxin. The mechanism of 1080 toxicity, susceptibility of target and non-target species, persistence of 1080 in the environment and risk of accidental poisoning are discussed. Particular emphasis is placed on 1080 toxicity in the dog. Early recognition of intoxication is most important for prognosis and relies upon characteristic clinical signs and diagnostic findings. The treatment of 1080 intoxication remains a challenge with no proven antidotes. However, there are possible benefits from monoacetin, acetamide, calcium salts, colestipol, activated charcoal, peritoneal dialysis, sodium bicarbonate, neurotransmitter modulators and four-methylpyrazole. A recommended treatment protocol for 1080 toxicosis in dogs is included. Safety measures such as the use of wire dog muzzles and investigating alternatives to 1080 in pest control programs may be the key to reducing the incidence of future accidental poisonings.

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“…Na terapia de suporte, são utilizadas medicações que controlam as convulsões, com auxílio da intubação e ventilação (Osweiler 1996). Uma grande variedade de potenciais antídotos têm sido estudada, em especial, em ratos e camundongos, incluindo o monoacetato de glicerol (Rammell & Livingstone 1985), acetamida (Egyed & Schultz 1986, Górniak et al 1994, sais de cálcio (Shapira et al 1980), gluconato de cálcio associado ao a-cetoglutarato de sódio e succinato de sódio (Omara & Sisodia 1990), bicarbonato de sódio (Churchill 1996), agentes moduladores de neurotransmissores (Cook et al 2001) e 4-metilpirazole (Feldwick et al 1997).…”

Section: Terapêutica Da Intoxicação Por Monofluoroacetatounclassified

“…O monoacetato de glicerol é considerado o agente protetor mais eϐicaz em casos de intoxicação por ϐluoroacetato em ratos, coelhos, cães e macacos Rhesus (Chenoweth et al 1951, Rammell & Livingstone 1985, quando administrado precocemente, na dose de 0,5mg/kg/hora, por via intravenosa ou intramuscular até 20 minutos após a intoxicação (Mount 1992).…”

Section: Terapêutica Da Intoxicação Por Monofluoroacetatounclassified

Intoxicação por monofluoroacetato em animais

et al. 2011

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O monofluoroacetato (MF) ou ácido monofluoroacético é utilizado na Austrália e Nova Zelândia no controle populacional de mamíferos nativos ou exóticos. O uso desse composto é proibido no Brasil, devido ao risco de intoxicação de seres humanos e de animais, uma vez que a substância permanece estável por décadas. No Brasil casos recentes de intoxicação criminosa ou acidental têm sido registrados. MF foi identificado em diversas plantas tóxicas, cuja ingestão determina "morte súbita"; de bovinos na África do Sul, Austrália e no Brasil. O modo de ação dessa substância baseia-se na formação do fluorocitrato, seu metabólito ativo, que bloqueia competitivamente a aconitase e o ciclo de Krebs, o que reduz produção de ATP. As espécies animais têm sido classificadas nas quatro Categorias em função do efeito provocado por MF: (I) no coração, (II) no sistema nervoso central (III) sobre o coração e sistema nervoso central ou (IV) com sintomatologia atípica. Neste trabalho, apresenta-se uma revisão crítica atualizada sobre essa substância. O diagnóstico da intoxicação por MF é realizado pelo histórico de ingestão do tóxico, pelos achados clínicos e confirmado por exame toxicológico. Uma forma peculiar de degeneração hidrópico-vacuolar das células epiteliais dos túbulos uriníferos contorcidos distais tem sido considerada como característica dessa intoxicação em algumas espécies. O tratamento da intoxicação por MF é um desafio, pois ainda não se conhece um agente capaz de reverte-la de maneira eficaz; o desfecho geralmente é fatal

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Treatment of 1080 poisoning in dogs with glycerol monoacetate

Cited by 7 publications

References 2 publications

Toxicology of fluoroacetate: a review, with possible directions for therapy research

Toxicology of fluoroacetate: a review, with possible directions for therapy research

Sodium monofluoroacetate (Compound 1080) poisoning in dogs

Intoxicação por monofluoroacetato em animais

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