Comparison of insulin hypoglycemia-induced and fluoroacetate-induced convulsions in gold thioglucose lesioned mice

Marrazzi, Mary Ann; Holliday, J. F.

doi:10.1016/0006-2952(81)90523-2

Cited by 9 publications

(7 citation statements)

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“…29 There was a gradual and transient hyperglycemia confirming the data reported in the literature. 7,9,10 The SFAC also increases the levels of serum glucose and glycogen, as well as the ammonia concentration, and brain convulsions occur by the decrease in cerebral energy supply. 7,9 The hyperglycemia can be a consistent finding in intoxication by SFAC, 9,10 due to increased levels of endogenous cortisol, which has hampered in their metabolism during intoxication.…”

Section: Discussionmentioning

confidence: 99%

“…7,9,10 The SFAC also increases the levels of serum glucose and glycogen, as well as the ammonia concentration, and brain convulsions occur by the decrease in cerebral energy supply. 7,9 The hyperglycemia can be a consistent finding in intoxication by SFAC, 9,10 due to increased levels of endogenous cortisol, which has hampered in their metabolism during intoxication. 9 Moreover, the animals of this study showed hypokalemia, hypophosphatemia, and hypomagnesemia, not described in literature.…”

Section: Discussionmentioning

confidence: 99%

“…[7][8][9] Body system thermo-regulation is also affected because of energy production block, resulting in hypothermia in cats and hyperthermia in dogs. 9,10 Hypocalcemia and hypokalemia are common, as well as hypotension and metabolic acidosis. 9 The oral toxic doses of SFAC in different species are 0.2-7 mg/kg in rodents, 0.5-2 mg/kg in human, 0.3-0.7 mg/kg in goats, 0.5-1.75 mg/kg horses, 0.3-0.4 mg/kg in pigs, 0.15-0.62 mg/kg in cattle, 0.25-0.5 mg/kg in sheep, 10-30 mg/kg in birds, 0.096-0.2 mg/kg in dogs and 0.3-0.5 mg/kg in cats.…”

Section: Introductionmentioning

confidence: 99%

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Hematological and biochemical profiles and histopathological evaluation of experimental intoxication by sodium fluoroacetate in cats

et al. 2010

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Sodium fluoroacetate (SFAC) is a potent rodenticide, largely used for rodent and domestic pest control. The toxic effects of SFAC are caused by fluoroacetate, a toxic metabolite, whose toxic action blocks the Krebs cycle and also induces the accumulation of citrate in the body, which is a serum calcium chelator. The most common clinical signs of this intoxication are the cardiac and neurological effects. However, the hematological, biochemical and histopathological findings occurring in intoxication are still unknown in different species. In the present study, 16 domestic cats were experimentally intoxicated with oral doses of fluoroacetate (0.45 mg/kg). The hematological and biochemical profiles and histopathological findings were made to look for auxiliary diagnosis methods in SFAC intoxications. The hematological profile showed transitory leucopenia and thrombocytopenia; in the biochemical profiles were detected hyperglycemia, increase of creatinequinase enzyme (CK) and creatinequinase cardiac isoenzyme (CK-MB), hypokalemia and hypophosfatemia. In the macroscopic and histopathological findings were observed lesions characteristic of degenerative and ischemic processes in heart, kidneys, liver, brain and lungs. These changes may be auxiliary to the diagnosis of intoxication by SFAC in cats, when associated with clinical signs described for the species. Thus, the complete blood count with platelet count, serum glucose, enzymes CK and CK-MB isoenzyme, as well as the electrolytes potassium and phosphorus, can facilitate the laboratory diagnosis during intoxication by SFAC, associated with the pathological findings in the case of death of the intoxicated animal.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hematological and biochemical profiles and histopathological evaluation of experimental intoxication by sodium fluoroacetate in cats

et al. 2010

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“…Convulsões induzidas pela hipoglicemia insulínica diferem daquelas provocadas por MF. No primeiro caso, ocorre redução da concentração de glicose para o sistema nervoso central (SNC); já a intoxicação por MF causa o bloqueio especíϐico do ciclo de Krebs e as convulsões são decorrentes do reduzido suprimento energético ao SNC (Marrazzi & Holliday 1981). Em coelhos, a convulsão e ϐibrilação ventricular iniciam-se, em geral, após um estímulo externo ou pela contenção dos animais; tal constatação, sugere que o aumento na liberação de catecolaminas durante a intoxicação pode exercer um fator desencadeador das alterações cardíacas nestes animais (Huang et al 1980).…”

Section: Toxicidade De Monofluoroacetatounclassified

“…A hiperglicemia pode ser um achado signiϐicativo na intoxicação por este composto (Marrazzi & Holliday 1981). Esta é decorrente do aumento dos níveis de cortisol endógeno, que tem seu metabolismo prejudicado pela diminuição dos níveis de ATP necessários para a metabolização da substância no ϐígado (Ballard & Hyde 1967).…”

Section: Diagnósticounclassified

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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Effects of bipiperidyl mustard (BPM) lesions on insulin hypoglycemic convulsions

Holliday

Fish

Churchill

et al. 1982

Physiology & Behavior

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Comparison of insulin hypoglycemia-induced and fluoroacetate-induced convulsions in gold thioglucose lesioned mice

Cited by 9 publications

References 9 publications

Hematological and biochemical profiles and histopathological evaluation of experimental intoxication by sodium fluoroacetate in cats

Hematological and biochemical profiles and histopathological evaluation of experimental intoxication by sodium fluoroacetate in cats

Intoxicação por monofluoroacetato em animais

Effects of bipiperidyl mustard (BPM) lesions on insulin hypoglycemic convulsions

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