61 



The same comparisons are presented for EL4 cells in 

 Table 2. As was observed for CHO cells, free a-amanitin 

 is more effective in inhibiting cell growth than is conju- 

 gated a-amanitin with about three fold greater inhibition 

 seen at 5 x 10 M a-amanitin for nonconjugated toxin. EL4 

 cells were approximately five times less sensitive to a- 



amanitin in either form than were CHO cells. Although the 



3 

 H-TdR data presented parallels, the cell number data with 



a-amanitin being more inhibitory than ADH-BSA at equivalent 



concentrations, EL4 cells did not incorporate exogenous 



thymidine to any great extent under the conditions examined. 



The data is presented only for comparative purposes. 



Table 3 contains similar inhibition data for AV3 cells. 

 Like EL4 cells, AV3 did not incorporate exogenous thymidine 

 to a significant extent but the inhibition obtained paral- 

 leled the cell number data. For AV3 however, inhibition of 

 cell proliferation by ADH-BSA was strikingly different than 

 that observed in CHO and EL4 cells. Although AV3 cells are 

 equally as sensitive to free a-amanitin as are CHO cells, 

 the AV3 cells were eight times more susceptible to conju- 

 gated a-amanitin in comparison to an equivalent molar dose 

 of free a-amanitin. This would imply a preferential uptake 

 of ADH-BSA by AV3 and/or modification of the conjugate to 

 a more toxic derivative after uptake by AV3 cells. 



Figure 8 depicts cell size distributions of AV3 , CHO 

 and EL4 cells after 48 hours of exposure to ADH-BSA or 

 a-amanitin. The results clearly indicate that no shift in 



