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