27 

 were not different (P > .05) among treatments. Concentrate 

 intakes were similar for all groups with no anorexia noted. 



There were no treatment differences (P > .05) in serum Zn 

 content for all days of collection (Figure 3-1), with the 

 amount of dietary Zn not playing any role in controlling serum 

 Zn, since the unsupplemented controls were not different. 

 Surprisingly, on d 28 (beginning of depletion phase) serum Zn 

 in most treatments (including the control) started increasing 

 and upon repletion (d 56) levels started falling again. As 

 with serum Zn, erythrocyte Zn was not affected (P > .05) by 

 treatment (Figure 3-2) . Unlike serum Zn, however, Zn content 

 of erythrocytes dropped in all treatments with depletion and 

 stabilized with repletion. 



Overall mean serum Cu concentrations fluctuated greatly 

 but tended to decrease with all Zn treatments (Figure 3-3) . 

 By d 56 the Cu concentration increased (from d 1) by .17 ± .07 

 |ig/ml (mean ± SEM) for ZnO treatment and was greater (P < .05) 

 than both ZnMet and control treatments which dropped by -.04 

 ± .05 and -.05 ± .07 (ig/ml, respectively. By d 70 the Cu 

 concentrations for the ZnO treated sheep (-.02 ± .13) had 

 decreased less (P < .05) than other treatments. 



There were no treatment differences (P > .05) in Zn 



(Table 3-2) and Cu (Table 3-3) tissue concentrations and 



liver, kidney and pancreas MT concentrations (Table 3-4) . As 



with the blood data, no differences were seen among Zn sources 



or even between the supplemented treatments and the 



