12 OLOV LINDBERG et ul. 



It was shown previously that amytal inhibits shghtly the dinitro- 

 phenol-induced ATPase [75], and that this inhibition can be greatly 

 potentiated if a stimulating concentration of atebrin [76] or chlorpromazine 

 [77] is added. Fig. 7 illustrates this effect and shows that a similar poten- 

 tiation did not occur with azide or desaminothyroxine. In fact, des- 

 aminothyroxine seemed even to eliminate the slight inhibition given by 

 amytal. 



log M 



Fig. 6. Comparison of effects of azide, atebrine, chlorpromazine and desamino- 

 thyroxine on the dinitrophenol-induced ATPase activity of rat liver mitochondria. 

 Experimental conditions as in Fig. i . 



An interesting effect of atebrin was discovered by observing that this 

 compound in a concentration of o • 5 mM was able to relieve almost com- 

 pletely the inhibitory effect of desaminothyroxine on the dinitrophenol- 

 induced ATPase reaction (Table I). Peculiarly enough, this effect of 

 atebrin was not shared by chlorpromazine. Similarly, no atebrin-like 

 effect was found with flavin nucleotides. 



It appeared from the above findings that the effect of desaminothy- 

 roxine on the dinitrophenol-induced ATPase clearly differed from those 

 of the flavin antagonists, whereas the difference from that of azide was less 

 obvious. However, a clear-cut distinction was found also between des- 

 aminothyroxine and azide in the effects of the inhibitors on the Mg + +- 

 activated ATPase of the Kielley and Kielley preparation. As was reported 

 previously [76], the Mg "^ -activated ATPase is characterized by a stimula- 

 tion, up to about 50*)^, by 0"5-i niM sodium dithionite. This compound, 

 however, not only stimulates the Mg + +-activated ATPase reaction but 



