Distribution of Radioactive Cobalt in the Rat

Cuthbertson, William; Free, Audrey A.; Thornton, Doreen M.

doi:10.1079/bjn19500007

Cited by 18 publications

(4 citation statements)

References 4 publications

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“…The paradox that cobalt, which is such a toxic substance, may still give rise to erythrocytosis with a greatly stimulated bone marrow activity is probably due to the distribution of cobalt in the organism. As shown in several independent studies, cobalt is concentrated in the kidney, mainly in the corticomedullary zone, whereas the amount in the bone marrow is low (Copp & Greenberg, 1941;Berlin, 1950;Cuthbertson et al, 1950;Carlberger, 1961;Flodh, 1968;Lindgren & Salmi, 1968). The systemic toxicity is rather brief since cobalt is quickly eliminated through the urine and the released erythropoietin from the more severely hit kidney cells may, therefore, act on fairly protected and uninhibited bone marrow cells.…”

Section: Discussionmentioning

confidence: 91%

A Comparison of the Cobalt, Methylene Blue, Zinc, Arsenite and Amino Triazole Effect on Erythropoietin Production

1973

Br J Haematol

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The possible mechanisms of action of cobalt in stimulating erythropoietin production are considered.It is demonstrated that although arsenite shares some ofits biochemical effects with cobalt, it does not stimulate the production of erythropoietin. It has been claimed previously that methylene blue could prevent the development of erythrocytosis after cobalt. In the present series of experiments, however, methylene blue did not affect the production of erythropoietin after injection of cobalt to rabbits.

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Section: Discussionmentioning

confidence: 91%

A Comparison of the Cobalt, Methylene Blue, Zinc, Arsenite and Amino Triazole Effect on Erythropoietin Production

1973

Br J Haematol

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“…These efforts a t biosynthesis were unsuccessful, but they did provide information on the distribution of cobalt in the pig (6) and the rat. (6) Since crystalline insulin had been shown in 1933 to be a salt of insulin and a bivalent metal such as cobalt, ULRICH and COPP") cornpared the mctabolism of 6oCoCI, in normal and alloxandiabctic rats.…”

mentioning

confidence: 94%

“…(6) Since crystalline insulin had been shown in 1933 to be a salt of insulin and a bivalent metal such as cobalt, ULRICH and COPP") cornpared the mctabolism of 6oCoCI, in normal and alloxandiabctic rats. No diffcrences in distribution were found, although a high conccntration of cobalt in pancreas, liver, and kidney was notcd.…”

mentioning

confidence: 99%

Radiation Dosimetry of Internal Contamination by Inorganic Compounds of Cobalt

Hollins¹,

McCullough²

1971

Health Physics

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The whole body retention of cobalt during a period of 400 days after injection of CoCl, has been determined for a strain of specific-pathogen-free albino rats. The method used to fit both exponential and power functions to the data and the application of statistical tests which justify the selection of a function with five exponential terms as the best fit are dcscribed. The statistical mcthods used in this paper are presentcd in detail because of their possible application to other studics of a similar nature.Thc amounts of cobalt in 19 tissucs havc been measured at various times and expressed as concentration factors, which were found to be stablc during the period between 10 and 72 days after injection. However, the concentration factor of bone increascd during a period of400 days at thc cxpense of thc concentrations in the soft tissues. The function developed to dcscribc the whole body retention of cobalt is substantially dilfercnt from that selectcd in ICRP Publication 10 and examplcs of the consequences of applying the two functions to the radiation dosimetry of internal contamination by 6oCoCl, are given. The selection of critical organs for radioisotopes of cobalt is also discussed.

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“…Cobalt salts have been given orally to human subjects in doses up to 150 mg of cobaltous chloride daily without clearly pronounced harmful effects (Davis & Fields, 1955). Orally administered cobalt is very slightly absorbed, and mainly excreted in the faeces; injected intravenously it is mainly, and rapidly, excreted in the urine (Taylor, 1962); according to experiments with radioactive 60Co (Cuthbertson, Free & Thornton, 1950) what remains in the body is to be found mainly in liver, kidneys, pancreas and spleen.…”

Section: The Toxicity Of Cobalt Saltsmentioning

confidence: 99%

Cobalt Compounds as Antidotes for Hydrocyanic Acid

Evans

1964

British Journal of Pharmacology and Chemotherapy

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The antidotal potency of a cobalt salt (acetate), of dicobalt edetate, of hydroxocobalamin and of cobinamide against hydrocyanic acid was examined mainly on mice and rabbits. All the compounds were active antidotes for up to twice the LD50; under some conditions for larger doses. The most successful was cobalt acetate for rabbits (5 x LD50), which was effective at a molar cyanide/cobalt (CN/Co) ratio of 5, but had as a side-effect intense purgation. Hydroxocobalamin was irregular in action, but on the whole was most effective for mice (4.5 X LDS0 at a molar ratio of 1), and had no apparent side effects. Dicobalt edetate, at molar ratios of up to 2, was more effective for rabbits (3 x LD50) than for mice (2 x LD50), but had fewer side effects than cobalt acetate. The effect of thiosulphate was to augment the efficacy of dicobalt edetate and, in mice, that of hydroxocobalamin; but, apparently, in rabbits, to reduce that of hydroxocobalamin. Cobinamide, at a molar ratio of 1, was slightly more effective than hydroxocobalamin on rabbits and also less irregular in its action. Cobalt acetate by mouth was effective against orally administered hydrocyanic acid. The oxygen uptake of the body, reduced by cyanide, is rapidly reinstated when one of the cobalt antidotes has been successfully administered.Hydrocyanic acid acts as a poison because it combines with, and immobilizes the function of, the iron atom in cytochrome oxidase (derived from cytochrome a3) (Keilin & Hartree, 1939), so blocking the electron transfer through the cytochrome system, and checking the final oxidations involving oxygen uptake of the tricarboxylic acid cycle. It also inhibits many other enzymes, for example, decarboxylases (Blaschko, 1942); these last effects have no recognizable relation to the toxic action.Attempts to find an antidote for cyanide have usually been in the direction of breaking down the cyanide-cytochrome a3 complex, and have looked for substances with a stronger affinity for cyanide ions than has the oxidase. One such method is to convert some of the blood haemoglobin into methaemoglobin, for example, by injection of a nitrite (Paulet, 1959); the methaemoglobin combines with the cyanide ion to form the very stable cyanmethaemoglobin. This has the drawback that it involves the loss of oxygen-carrying power of the blood, so that, for example, to antidote twice the LD50 of cyanide would be equivalent to the loss of about 10% (or in an adult man 450 ml.) of the blood.Since cobalt salts form stable complexes with cyanide, the cobaltocyanides, M4Co(CN)6, and the cobalticyanides, M3Co(CN)6, they have been shown long ago

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Distribution of Radioactive Cobalt in the Rat

Cited by 18 publications

References 4 publications

A Comparison of the Cobalt, Methylene Blue, Zinc, Arsenite and Amino Triazole Effect on Erythropoietin Production

A Comparison of the Cobalt, Methylene Blue, Zinc, Arsenite and Amino Triazole Effect on Erythropoietin Production

Radiation Dosimetry of Internal Contamination by Inorganic Compounds of Cobalt

Cobalt Compounds as Antidotes for Hydrocyanic Acid

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