Table 1.

Some contrasts in susceptibility of ruminants and humans to copper deficiency

Copper deficiency	Ruminants	Humans
Natural occurrence	Would be endemic in grazing livestock in some regions without regular use of copper supplements	Exceedingly rare: largely confined to individuals with genetic disorders; may occur in malnourished children
Unnatural occurrence	Induced by industrial or agricultural exposure to antagonists (e.g., iron, zinc) via exploitation of underground resources of minerals and water	Bariatric surgery reduces capacity to absorb copper and may in time cause copper-responsive neuropathy and anemia
Antagonism from molybdenum	Most common cause of clinical symptoms (hypocuprosis): these include retarded growth, bone deformities, loss of hair/wool strength and color, infertility, diarrhea; neuropathy in lambs when exposure is in utero; anemia in severe cases	Unrecorded
Copper reserves	Abundant in liver, including neonate	Meagre
Genetic variation	Breeds vary in susceptibility: high heritabilities for plasma and liver copper	Single gene mutations (e.g., Menkes disease: symptoms similar to young molybdenum- exposed ruminants); polymorphisms?
Hypocupremia	Marked tolerance	Tolerance unknown but probably low
Biochemical markers	Liver and plasma copper commonly relied on but imprecise: oxidase activity of ceruloplasmin unreliable	Oxidase activity of ceruloplasmin widely used as surrogate for plasma copper: more sensitive alternatives sought