Copper toxicity in a New Zealand dairy herd

Johnston, H.K.; Beasley, Laura J.; MacPherson, Neil

doi:10.1186/2046-0481-67-20

Cited by 27 publications

(28 citation statements)

References 8 publications

(5 reference statements)

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“…After adding ammonium molybdate, copper in blood and liver decreased, hemoglobin and red blood cell count content and glutathione peroxidase activity increased, and malondialdehyde and glutamic oxaloacetic transaminase activity decreased. This is consistent with the result of previous studies that molybdenum blocks copper absorption, highlighting the antagonism between molybdenum and copper, and forms thiomolybdate in the gastrointestinal tract [33][34][35], in addition to the formation of Cu-thiomolybdate complexes and Cu-Mo-S-protein compounds [36,37]. Cu-thiomolybdate complexes are insoluble and excreted directly from the intestinal tract, which blocks the absorption of copper, resulting in decreased copper levels.…”

Section: Discussionsupporting

confidence: 91%

Response of Wumeng Semi-Fine Wool Sheep to Copper-Contaminated Environment

Wu¹,

Shen²

2020

Pol. J. Environ. Stud.

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We evaluated the response of Wumeng semi-fine wool sheep to a copper-contaminated environment and found an action plan to solve copper pollution through a grazing experiment and ammonium molybdate supplementary experiment carried out in Weining County of Guizhou Province in China. The content of heavy metal element in soil, herbage, and animal tissues was measured by atomic absorption spectrometry, and the blood physiological and biochemical indicators were determined by animalspecific automatic blood analyzer and automatic biochemical analyzer respectively. The results showed that the copper content in soil and herbage of contaminated pasture was significantly higher than that in control pasture, and the copper content in blood and liver in affected sheep was significantly higher than that in the control group. Hemoglobin (Hb), red blood cell count (RBC), hematocrit (PCV), mean corpuscular volume (MCV) contents and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities in affected sheep were significantly lower than those in control, while the activities of ceruloplasmin (CP), glutamic oxaloacetic transaminase (GOT), creatine phosphokinase (CPK) and malondialdehyde (MDA) were significantly higher. There was no significant difference in the level of mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC) and white blood cell count (WBC) between the affected and control sheep. After supplementation of ammonium molybdate, copper content in blood and liver decreased gradually, and the abnormal blood indexes recovered. At the end of the ammonium molybdate supplementation experiment, Wumeng semi-fine wool sheep in the drug-control group (CK group) showed hemoglobinuria, jaundice, anemia and other symptoms. Conclusion: a copper-contaminated environment seriously affected mineral metabolism and blood physiological and biochemical indicators of Wumeng semi-fine wool sheep, and we can utilize the antagonism of molybdenum and copper in the diet to achieve the goal of harmless utilization of a copper-polluted meadow.

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Section: Discussionsupporting

confidence: 91%

Response of Wumeng Semi-Fine Wool Sheep to Copper-Contaminated Environment

Wu¹,

Shen²

2020

Pol. J. Environ. Stud.

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“… Bidewell and others (2012) recorded eight cows with chronic copper toxicity that had liver copper concentrations ranging from 8148 µmol/kg to 23493 µmol/kg DM (mean 14223.5 µmol/kg DM), whilst four herd mates with no clinical signs of chronic copper toxicity had liver copper concentrations of 5260, 9628, 10084 and 21850 µmol/kg DM. Similarly in New Zealand Johnson and others (2014) in an investigation into six deaths from chronic copper toxicity found the liver copper concentrations of 10 random herd mates to range from 1900 µmol/kg to 3500 µmol/kg wet weight with a mean of 2620 (±188) µmol/kg (6785 µmol/kg DM to 12500 µmol/kg DM, with a mean of 9357 (±671) µmol/kg assuming a DM of 280 g/kg). In only three of the dead cows were liver copper concentrations analysed and these were 2300 µmol/kg, 2400 µmol/kg, 2700 µmol/kg wet weight (8214 µmol/kg DM, 8571 µmol/kg DM, 9643 µmol/kg DM).…”

Section: Discussionmentioning

confidence: 97%

Liver copper concentrations in cull cattle in the UK: are cattle being copper loaded?

Kendall

Holmes-Pavord

Bone³

et al. 2015

Veterinary Record

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With the release of the Department for the Environment, Food and Rural Affairs/Advisory Committee on Animal Feed Guidance Note for Supplementing Copper to Bovines it was noted that the current copper status of the national herd was not known. Liver samples were recovered from 510 cull cattle at a single abattoir across a period of three days. The samples were wet-ashed and liver copper concentrations determined by inductively coupled plasma mass spectrometry analysis. Breed, age and previous location information were obtained from the British Cattle Movement Service. Dairy breeds had higher liver copper concentrations than beef breeds. Holstein-Friesian and ‘other’ dairy breeds had 38.3 per cent and 40 per cent of cattle above the Animal Health and Veterinary Laboratories Agency (AHVLA) reference range (8000 µmol/kg dry matter), respectively, whereas only 16.9 per cent of animals in the combined beef breeds exceeded this value. It was found that underlying topsoil copper concentration was not related to liver copper content and that age of the animal also had little effect on liver concentration. In conclusion, over 50 per cent of the liver samples tested had greater-than-normal concentrations of copper with almost 40 per cent of the female dairy cattle having liver copper concentrations above the AHVLA reference range, indicating that a significant proportion of the UK herd is at risk of chronic copper toxicity.

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“…In practice, most clinical episodes of chronic copper toxicity have affected dairy herds (e.g., [ 9 , 69 , 70 ]), and biomonitoring of copper concentrations in the liver under the suspicion of copper over-supplementation has shown that most of the herds that exceed the safe limits are also dairy herds [ 11 , 12 ]. However, these findings do not necessarily indicate that dairy-aptitude cattle are more susceptible to copper toxicity than beef-aptitude cattle, and higher copper supplementation in dairy herds may also be an important factor.…”

Section: Other Underlying Reasons: Breed Susceptibilitymentioning

confidence: 99%

Copper Supplementation, A Challenge in Cattle

López‐Alonso

Miranda

2020

Animals

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Ensuring adequate copper supplementation in ruminants is a challenging task due to the complexity of copper metabolism in these animals. The three-way interaction between copper, molybdenum and sulphur (Cu-Mo-S) in the rumen makes ruminants, particularly cattle, very susceptible to suffering from secondary copper deficiency. Paradoxically, excessive copper storage in the liver to prevent deficiency becomes a hazard when ruminants are fed copper-supplemented diets even slightly above requirements. While cattle were traditionally thought to be relatively tolerant of copper accumulation, and reports of copper poisoning were until recently somewhat rare, in recent years an increased number of episodes/outbreaks of copper toxicity in cattle, particularly in dairy cattle, have been reported worldwide. The growing number of lethal cases reported seems to indicate that copper intoxication is spreading silently in dairy herds, urging the development of strategies to monitor herd copper status and improve farmers’ awareness of copper toxicity. In fact, monitoring studies carried out on numerous samples collected from culled animals in slaughterhouses and/or diagnostic laboratories have demonstrated that large numbers of animals have hepatic copper concentrations well above adequate levels in many different countries. These trends are undoubtedly due to copper supplementation aimed at preventing copper deficiency, as dietary copper intake from pasture alone is unlikely to cause such high levels of accumulation in liver tissue. The reasons behind the copper overfeeding in cattle are related both to a poor understanding of copper metabolism and the theory of “if adding a little produces a response, then adding a lot will produce a better response”. Contrary to most trace elements, copper in ruminants has narrow margins of safety, which must also be formulated considering the concentrations of copper antagonists in the diet. This review paper aims to provide nutritionists/veterinary practitioners with the key points about copper metabolism in cattle to guarantee an adequate copper supply while preventing excessive hepatic copper loading, which requires à la carte copper supplementation for each herd.

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Copper toxicity in a New Zealand dairy herd

Cited by 27 publications

References 8 publications

Response of Wumeng Semi-Fine Wool Sheep to Copper-Contaminated Environment

Response of Wumeng Semi-Fine Wool Sheep to Copper-Contaminated Environment

Liver copper concentrations in cull cattle in the UK: are cattle being copper loaded?

Copper Supplementation, A Challenge in Cattle

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