Some effects of synthetic fluoro compounds on the metabolism of acetate and citrate

Gal, Emery M.; Peters, Rudolph; Wakelin, R. W.

doi:10.1042/bj0640161

Cited by 47 publications

(11 citation statements)

References 18 publications

(9 reference statements)

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“…As expected, the tissues of animals poisoned in vivo with fluorocitrate accumulated high levels of citrate (Gal, Peters and Wakelin, 1956;Gordon, 1961 ;Peters, 1965). Citrate accumulation is greater during fluorocitrate than during fluoroacetate poisoning (Dr P. B a a , 1969, personal communication), and the rise in citrate occurs earlier (Gal et d.).…”

Section: The Biochemical Lesionsupporting

confidence: 62%

Light‐ and electron‐microscope studies of the rat kidney after administration of inhibitors of the citric acid cycle in vivo: Changes in the proximal convoluted tubule during fluorocitrate poisoning

McDowell

1972

The Journal of Pathology

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Section: The Biochemical Lesionsupporting

confidence: 62%

Light‐ and electron‐microscope studies of the rat kidney after administration of inhibitors of the citric acid cycle in vivo: Changes in the proximal convoluted tubule during fluorocitrate poisoning

McDowell

1972

The Journal of Pathology

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“…Peters (9) has demonstrated that fluoroacetate is converted to fluorocitrate by biological systems, with consequent inhibition of the enzyme, aconitase. Other studies (19), however, indicated that these two compounds did not result in equivalent inhibitory activities when administered to rats.…”

Section: Discussionmentioning

confidence: 94%

The Metabolism of Citrate-C14 in Normal and in Fluoroinhibitor-Poisoned Rats*

Gordon¹

1961

J. Clin. Invest.

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A cyclical exchange of citrate has been shown to exist in the intact organism, with the blood plasma serving as the transporting medium. In vivo studies have indicated a considerable uptake of citrate by the liver (1) and kidney (2), and a release of citrate into the blood by the peripheral tissues (1, 3) and intestine (4,5). Interest in the blood citrate flux has centered primarily around the importance of this intermediate in carbohydrate metabolism, in its relationship to calcium mobilization and deposition in bone (6), and in its role as a chelating agent for calcium in the urine (7, 8).The studies reported here have been concerned with an attempt to elucidate the metabolic fate of the blood citrate in rats with the aid of radioactive citrate. The data, obtained by following the pattern of respiratory C140, and the urinary excretion of radioactive carbon after the intravenous administration of sodium citrate-1,5-C'4, indicated a rapid turnover of the blood citrate. Three hours after injection of the labeled citrate, approximately 90 per cent of the radioactivity was recovered in the respiratory CO., and in the urinary citrate. Evidence for the utilization of blood citrate as a precursor of tissue components was provided by assaying the C14 content of protein and lipid of kidneys and liver after intravenous citrate-C14 administration.In an effort to define further the metabolic fate of the blood citrate, inhibitors of citrate oxidation were administered prior to citrate-C14 administration. Peters (9) Fed, female Sprague-Dawley rats, weighing between 185 and 235 g, were used. Citric acid-1,5-C"' was obtained from Tracerlab, Inc., and sodium acetate--C1'4 from Volk Radiochemical Co. Sodium fluoroacetate 1 was purchased from Bios Laboratories, Inc. Barium fluorocitrate, synthesized by the method of Rivett (10), was obtained from the Sonbert Chemical Co., Brooklyn, N. Y.; this preparation contained less than 1 per cent barium citrate by specific analysis. Before use, the barium salt was dissolved in dilute HCl, the barium was precipitated with saturated sodium sulfate and the supernatant fluid was neutralized with dilute NaOH. Solutions of the fluoroinhibitors were freshly prepared prior to use.In the in vivo experiments, sodium citrate-1,5-C"4 in isotonic saline was given intravenously in a volume of 0.3 ml. Collection of respiratory CO2 was accomplished by drawing CO2-free air through a glass metabolism jar containing the rat, and the respiratory CO2 was trapped in NaOH. Barium carbonate precipitates were prepared from aliquots of the NaOH solutions. After the BaCO3 was washed with water and then alcohol, it was plated and counted in a Nuclear-Chicago gas-flow counter with a Micromil window. Urine collections were made up to standard volume, and aliquots were taken for direct plating and for conversion of the carboxyl groups of the urinary citrate to CO2 with ceric sulfate (11); the CO2

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“…Ocorre diminuição do metabolismo de todos os substratos provenientes da oxidação de carboidratos, proteínas e lipídios no ciclo de Krebs com conseqüente acúmulo de ceto-substâncias no sangue. O citrato, por sua vez, acumulado no organismo, exerce principalmente um efeito quelante sobre o cálcio sérico levando à hipocalcemia, além dos efeitos cardiotóxicos e neurotóxicos do fluoroacetato 2 .…”

Section: Introductionunclassified

Variabilidade clínica na determinação da dose tóxica oral em intoxicação experimental por fluoroacetato de sódio em gatos

Collicchio-Zuanaze

Sakate

Crocci

2006

Braz. J. Vet. Res. Anim. Sci.

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O fluoroacetato de sódio (FAS) ou composto 1080 é um potente rodenticida utilizado no controle de roedores e predadores mamíferos. Sua utilização está proibida por lei em diversos países devido à sua alta toxicidade, mas no Brasil há evidências do uso ilegal e sem critérios causando intoxicações, principalmente em crianças e animais domésticos. O FAS age por meio do seu metabólito tóxico, o fluorocitrato, no bloqueio do ciclo de Krebs com conseqënte diminuição da produção de energia do organismo, provocando principalmente manifestações clínicas neurológicas e cardíacas. No presente estudo compararam quatro doses orais tóxicas do fluoroacetato de sódio, descritas em gatos, na literatura, observando-se o aparecimento dos sinais clínicos predominantes da intoxicação, as diferenças entre as doses quanto a variabilidade clínica em relação ao período de latência para o aparecimento dos sinais clínicos e sua respectiva intensidade. A dose oral tóxica que melhor caracterizou o quadro clínico da intoxicação por FAS em gatos, sem causar a letalidade aguda, foi de 0,45mg/kg. As diferenças entre as manifestações clínicas foram dose-dependentes e em ordem crescente de intensidade, caracterizando-se como sinais leves (dose 1: 0,3mg/kg), leves a moderados (dose 2: 0,4mg/kg), moderados a graves (dose 3: 0,45mg/kg) e graves (dose 4: 0,5mg/kg). Houve também variabilidade clínica individual entre animais intoxicados com a mesma dosagem do tóxico.

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Some effects of synthetic fluoro compounds on the metabolism of acetate and citrate

Cited by 47 publications

References 18 publications

Light‐ and electron‐microscope studies of the rat kidney after administration of inhibitors of the citric acid cycle in vivo: Changes in the proximal convoluted tubule during fluorocitrate poisoning

Light‐ and electron‐microscope studies of the rat kidney after administration of inhibitors of the citric acid cycle in vivo: Changes in the proximal convoluted tubule during fluorocitrate poisoning

The Metabolism of Citrate-C14 in Normal and in Fluoroinhibitor-Poisoned Rats*

Variabilidade clínica na determinação da dose tóxica oral em intoxicação experimental por fluoroacetato de sódio em gatos

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