Pathological consequences of copper deficiency and cobalt deficiency.
Aspects of the pathology of copper deficiency in several species, and cobalt deficiency in sheep, are summarized. An attempt is made to interpret morphological changes in copper-deficient animals in terms of biochemical defects. The common denominator may be mitochondrial lesions, with a generalized effect on energy-dependent synthetic functions of the cell. In copper deficiency, such defects can be attributed to depletion of copper-dependent enzymes, while deficiency of cobalt in ruminants is, in effect, deficiency of vitamin B12. The pathological consequences of vitamin B12 deficiency form a syndrome, notable features of which are neurological and muscular lesions, in which the metabolic consequences of hepatic damage may play a significant role.
D000748:Anemia, Macrocytic / Q000209:etiology; D000818:Animals; D003035:Cobalt / Q000172:deficiency*; D003300:Copper / Q000172:deficiency*; D005227:Fatty Acids / Q000378:metabolism; D006801:Humans; D008563:Membrane Lipids / Q000378:metabolism; D008765:Methylmalonyl-CoA Mutase / Q000172:deficiency; D008928:Mitochondria / Q000502:physiology / Q000648:ultrastructure; D010182:Pancreatic Diseases / Q000209:etiology / Q000503:physiopathology; D012636:Secretory Rate; D012756:Sheep; D012757:Sheep Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology
D005227:Fatty Acids; D008563:Membrane Lipids; D003035:Cobalt; D003300:Copper; D008765:Methylmalonyl-CoA Mutase