52 

 for 14 d prior to death. Animal 46 (CuLys) was slaughtered on 

 d 43 after it had only been eating 25 g/d for 5 d. Animal 1 

 (CuLys) was slaughtered on d 78 after it had only been eating 

 3 g/d for 7 d. The ewe lamb (288, CuSOJ never showed 

 anorexia or any other sign which reflected a Cu toxicity and 

 was slaughtered with the last animal to end the experiment. 



Overall, serum Cu concentrations rose sharply in all 

 animals, except 288 (CuS0 4 ), shortly before death (Figure 5- 

 1) . For two of the animals (1, CuLys and 77, CuS0 4 ) there was 

 a sharp decrease in serum Cu immediately before death. There 

 were no plateaus in the serum Cu response curve of animal 77 

 which might indicate a decreased ability to control serum Cu 

 concentration when compared to animals 1 and 46 (CuLys) . 



Overall, serum Zn (Figure 5-2) concentrations fluctuated 

 greatly for all animals but were mostly above the .65 (ig/ml 

 suggested by McDowell et al . (1984) where a deficiency might 

 be expected. It is also interesting that for the two CuLys 

 treated sheep, serum Zn concentrations fell dramatically 

 before death. The other animal (77) that exhibited signs of 

 Cu toxicity showed low concentrations but also a rise right 

 before death. 



In general, blood HCT (Figure 5-3) started rising before 

 death for three of the animals (1, 77 and 288) . For the 

 animal that died of natural causes, the blood HCT fell 

 dramatically before death. 



