17 

 One of the most powerful antagonists of Cu absorption in 

 general seems to be Zn (O'Dell, 1985) . Excess dietary Zn has 

 been reported to aggravate the signs of low Cu status (L'Abbe 

 and Fischer, 1984) . In rats fed adequate Cu levels (6 mg/kg) , 

 Zn dietary concentrations of 120 and 240 mg/kg depressed the 

 activities of important cuproenzymes such as liver superoxide 

 dismutase and heart cytochrome C oxidase (L'Abbe and Fischer, 

 1984) . This antagonistic effect appears to take place mainly 

 in the intestinal mucosa via MT (Cousins, 1985) . 



Transport and Tissue Uptake 



As with Zn, albumin appears to be the main Cu carrier in 

 portal blood. After passing through enterocytes, Cu is 

 transported through portal blood as a histidine-Cu-albumin 

 complex (Lau and Sarkar, 1971). There are controversial 

 reports as to the actual carrier of Cu in peripheral 

 circulation. After transport into hepatocytes, Cu is released 

 into the blood stream bound mostly to ceruloplasmin . Copper 

 seems to stay bound to ceruloplasmin through peripheral 

 circulation (O'Dell, 1990). Bremmer (1980), however, suggests 

 that the principal transport forms of Cu are its loosely bound 

 complexes with albumin and, to a lesser extent, to selected 

 amino acids which include histidine, threonine and glutamine. 

 Hepatic Cu is temporarily stored complexed to ceruloplasmin 

 and released into plasma or bile as such (Bremmer, 1980) . 



