Abstract
Simple SummaryCopper supplementation in ruminants deserves special attention because of the narrow margin between deficiency and toxicity, both of which ruminants are susceptible to suffering from. Supplementation of copper above requirements to prevent deficiency has led to an increased number of outbreaks of copper toxicity being reported in recent years, particularly in dairy cattle. In this paper we describe the key points of copper metabolism in cattle that should be taken into consideration to guarantee an adequate copper supply while preventing toxic effects.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.
Highlights
Copper (Cu) is an essential element for life and is required as a co-factor in hundreds of enzymatic reactions involved in red blood cell production, energy manufacturing, hormone formation, collagenAnimals 2020, 10, 1890; doi:10.3390/ani10101890 www.mdpi.com/journal/animalsAnimals 2020, 10, 1890 synthesis and protection against oxidative damage
While acute copper toxicosis can occur after administration of a large dose of copper, copper toxicosis is usually a chronic process that occurs when excessive copper is supplied in the diet and hepatic copper reserves are overwhelmed [6]
Traditionally only young calves were considered sensitive to copper, and adult cattle were thought to be quite tolerant to copper [9], recent episodes of chronic copper toxicity have mostly been seen in dry dairy cattle, and changes in social groups and the weight loss associated with liver catabolism triggered by abrupt withdrawal of concentrates have been suggested to be the main stressors [9,10]
Summary
Copper (Cu) is an essential element for life and is required as a co-factor in hundreds of enzymatic reactions involved in red blood cell production, energy manufacturing, hormone formation, collagen. Sheep are the most susceptible to chronic copper toxicity, and farmers/nutritionists are aware that over supplementation with copper must be avoided to prevent excessive hepatic copper accumulation. This can be challenging as under some circumstances dietary copper requirements in sheep may overlap with levels that are toxic under other circumstances. Holstein Friesian [11,15] and Jersey cows [12,21], and available temporal data show an alarming tendency for an increasing incidence of cases [12] 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 accumulation in liver tissue [22]. À la carte copper supplementation is required for each herd
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