60 

 they were euthanized after anorexia had been seen for several 

 days . 



The CK analysis reflects myodegradation (Meyer et al . , 

 1992) in animals 1 and 77 prior to death which might have been 

 caused by the excess Cu in the blood being picked up by the 

 muscle and rupturing the cells. The release of GGT from the 

 hepatic cells of animal 77 was greater than that of all other 

 animals. The increased GGT activity represents a cholestasis 

 (Meyer et al . , 1992) by d 13 for all Cu affected animals. It 

 was interesting to see animals 46 and 1 survive longer with 

 such high levels of serum GGT as compared to 77 . The source 

 of the high AST levels is the liver (Duncan and Prasse, 1977) . 

 A rapid increase occurred in animal 77 and a slower one for 

 animals 1 and 46 which is proportional to the number of 

 hepatocytes damaged. Animal 1 seems able to recover from the 

 original cholestasis due to decreased AST levels. 



The heinz bodies seen in animal 77 before death 

 represents an increased hemoglobin turnover (Meyer et al . , 

 1992) resulting from the hemolytic crisis. The yellow colored 

 serum appearing before death may be an accumulation of bile 

 acids and bilirubin (also due to hemolytic crisis) in 

 peripheral circulation but these tests were not conducted. It 

 is necessary to conduct another trial to determine MT levels 

 of animals supplemented with CuLys to evaluate the relatively 

 increased survivability of those animals. 



