119 



quantitated by determining cell numbers as a function of 

 increasing concentrations of each inhibitor to which the 

 cells had been exposed. Figure 26 shows the results 

 expressed as a percentage of the control number. Free 

 ADGG had little effect on the growth of the cells after a 

 15 minute exposure to concentrations as high as 3 x 10 M. 

 Con A had no effect up to 40yg/ml but at 120ug/ml resulted 

 in 30% inhibition of cell growth. ADGG-Con A had a remark- 

 able effect at a concentration as low as 0.5 x 10 M with 

 respect to amanitin where greater than 50% inhibition of 

 cell growth was observed. At the maximum dose tested, 

 3 x 10 M, ADGG-Con A caused 80% inhibition of cell growth. 



The concentration of conjugated ADGG that resulted in 50% 



-7 

 inhibition (50% inhibitory does, ID,..) was 2.1 x 10 M. 



At that concentration, free ADGG or the equivalent amount 



of Con A to that present in the conjugate, had no effect. 



In another experiment, the inhibition of H-7 cell 

 growth obtained by an ADGG-Con A concentration of 1 x 10 M 

 was prevented by exposing the cells to the conjugate in the 

 presence of the Con A specific sugar, MDM (l.OmM). MDM 

 by itself caused no effect, 1 x 10 m ADGG-Con A caused 

 58% inhibition and cells protected with MDM had only 6.7% 

 inhibition. 



These results were compared to the effects of contin- 

 uous exposure of H-7 CHO cells to a-amanitin or ADGG for 

 48 hours shown in Figure 27. Alpha-amanitin resulted in 

 50% inhibition at a concentration of 0.5 x 10 M whereas 



