An investigation of the effects of intravenous administration of thiomolybdate on copper metabolism in chronic Cu-poisoned sheep

Gooneratne, Ravi; Howell, John C.; Gawthorne, J. M.

doi:10.1079/bjn19810055

Cited by 67 publications

(31 citation statements)

References 30 publications

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“…Copper toxicity is common is sheep, apparently because of their inability to excrete excess Cu from the body (Gooneratne et al 1985a). Copper toxicity in sheep is of major concern in Australia (Bull et al 1956),…”

Section: Canadian Journal Of Antmal Sciencementioning

confidence: 99%

Review of Copper Deficiency and Metabolism in Ruminants

Gooneratne¹,

Buckley²,

Christensen³

1989

Can. J. Anim. Sci.

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141

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The importance of copper (Cu) for the proper functioning of many biological systems is well recognized. Copper deficiency significantly affects ruminant livestock production in large areas of Canada as well as many other parts of the world. Selected aspects of recent research into Cu deficiency in ruminants have been reviewed, including the biochemistry and physiology of Cu deficiency as well as the metabolism of Cu. Because of the wide occurrence of Cu deficiency in ruminants grazing in areas of high molybdenum (Mo) and/or sulfur (S), research on the mechanisms of interference in Cu metabolism has received wide attention. Similarities in the physiological effects of the combination of molybdate and sulfide (or sulfate) and of thiomolybdates in ruminants, strongly suggest that thiomolybdates are primarily involved in the induction of Cu deficiency. Thiomolybdates appear to induce Cu deficiency by (i) limiting Cu absorption, (ii) binding Cu in albumin, thus delaying Cu uptake by the liver, (iii) depleting liver Cu, (iv) altering liver Cu and Cu from other tissues to a less available form, (v) increasing biliary Cu excretion, (vi) limiting reabsorption of biliary Cu, (vii) increasing urinary Cu excretion, and (viii) increasing endogenous secretion of Cu. Copper, S and/or Mo have also been identified as factors in the etiology of polioencephalomalcia and abmosal ulcers but the mechanisms involved are not clear. Key words: Ruminants, copper, defiency, metabolism, sulfur

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Section: Canadian Journal Of Antmal Sciencementioning

confidence: 99%

Review of Copper Deficiency and Metabolism in Ruminants

Gooneratne¹,

Buckley²,

Christensen³

1989

Can. J. Anim. Sci.

Self Cite

141

View full text Add to dashboard Cite

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“…There are conflicting reports in the literature regarding the ability of tetrathiomolybdate to increase copper excretion in the urine 3,9,14 , but in this experiment the molybdate therapy did not significantly increase cupruresis in relation to the other groups (Fig. 4).…”

Section: Discussionmentioning

confidence: 51%

“…Intravenously administered thiomolybdate increases plasma copper to very high levels, but most of the copper is then protein-bound and thus insoluble in trichloro-acetic acid (TCA) 9,11 . It is surmised that the TCA-insoluble copper is not taken up by red blood cells and this inability to penetrate erythrocytes is the reason why haemolysis is not precipitated and increased urinary copper excretion occurs 9 .…”

Section: Introductionmentioning

confidence: 99%

“…It is surmised that the TCA-insoluble copper is not taken up by red blood cells and this inability to penetrate erythrocytes is the reason why haemolysis is not precipitated and increased urinary copper excretion occurs 9 . Other researchers reported that tetrathiomolybdate treatment had no effect on the rate and amount of copper excreted in the urine 3,14 .…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of a commercially available molybdate formulation and zinc oxide boluses in preventing hepatic copper accumulation and thus enzootic icterus in sheep

Botha¹,

Shakespeare²,

Gehring³

et al. 2001

J. S. Afr. Vet. Assoc.

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The efficacy of a molybdate formulation and a zinc oxide bolus as prophylactic agents for enzootic icterus was evaluated in sheep. Before copper loading, liver biopsies were performed on 12 male, 6-month-old, Mutton Merino sheep to determine hepatic copper (Cu) and zinc (Zn) concentrations. The animals were restrictively randomised according to liver copper concentrations to 3 treatment groups (n = 4) to achieve similar mean liver copper concentrations per group. All sheep received 4 m /kg of a 0.5 %aqueous solution of CuSO4Â·5H2O intraruminally 7 days per week for 10 weeks. On Day 0 the sheep in the Mo-group were injected subcutaneously with 42 mg molybdenum (Mo) contained in a commercial molybdate formulation. The animals in the Zn-group each received a zinc oxide bolus, containing 43 g zinc oxide, via a rumen cannula. Treatment was repeated on Day 42. Four animals served as untreated controls. Urinary copper excretion, plasma copper concentration, haematocrit and glutamate dehydrogenase (GLDH) activity were determined throughout the trial. The animals were sacrificed after 10 weeks and liver samples were submitted for histopathological examination. Liver and kidney copper and zinc concentrations were determined. Neither the molybdate treatment nor the zinc oxide boluses prevented hepatic copper accumulation. The urinary copper excretion, plasma copper concentration, haematocrit and GLDH activity were not significantly different (P > 0.05) from the controls.

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“…Among the various thiomolybdates TM is the most potent. TM is toxic toward animals, but all the toxic effects are due to copper deficiency and are reversed by copper supplementation [258][259][260][261][262][263]. TM, extensively studied in sheep, acts as anticopper agent by forming mixed copper complexes with proteins.…”

Section: Tetrathiomolybdatementioning

confidence: 99%