78 J. B. CHAPPELL 



immeasurably small endogenous respiration, preincubation with arsenate 

 and DNP did not induce a requirement for ATP for succinate oxidation. 

 However, when 0-5 mM malate was present during the preincubation 

 period, the situation was exactly the same as it was with liver mitochondria, 

 namely ATP was required before succinate was oxidized at significant 

 rates and the addition of amytal at zero time, which of course prevented the 

 oxidation of malate, abolished the requirement for ATP. It is a reasonable 

 hypothesis therefore that when liver mitochondria are preincubated with 



Kidney 

 Mitochondria 



1 2 3 4 5 

 Time (mm) 



Fig. 8. Effect of arsenate and oxaloacetate on succinate oxidation by kidney 

 mitochondria. The oxaloacetate concentration was i mM, other conditions as for 

 Fig. 7. The early parts of the traces and the additions made, were the same in all 

 cases, but are not shown for the two traces on the right. 



arsenate and DNP the endogenous substrates give rise to oxaloacetate 

 which is responsible for the inhibition of succinate oxidation. This effect 

 can be demonstrated directly with kidney mitochondria (Fig. 8). In this 

 case, when DNP, arsenate and oxaloacetate were added before the succinate, 

 ATP was required for maximal rates of oxidation. Oxaloacetate had no 

 efi"ect in the absence of arsenate. The amount of oxaloacetate required to 

 produce this effect was about i mM, which was 40-100 times greater than 

 the amount of oxaloacetate which can be calculated to have arisen from 

 added malate in the experiment described above. It is possible that 

 enzymically generated oxaloacetate is more effective because it is produced 



