REGULATORY MECHANISMS IN ENERGY METABOLISM 147 



Similar results were obtained by Balasz (1959) in glycolyzing 

 brain mitochondria. In fortified systems the glycolysis was inhib- 

 ited, apparently due to inhibition or inactivation of triose phosphate 

 deh\ droijenase. 



Accumulation of an Inhibitor. It has been observed that the 

 addition of liver mitochondria to a glycolyzing brain supernatant 

 results in a strong inhibition of glycolysis (Aisenberg et al, 1957; 

 Aisenberg and Potter, 1957). In this system competition for phos- 

 phate acceptance was probably not involved, since the effect could 

 be seen with non-phosphorylating mitochondria (Aisenberg and 

 Potter, 1957 ) . The observations were explained by the maintenance 

 of a high level of TPN and consequent accumulation of 6-phospho- 

 gluconic acid. This results in inhibition of phosphofructokinase, 

 which in turn results in levels of glucose-6-phosphate which are in- 

 hibitory to hexokinase (Potter and Niemeyer, 1959). A similar re- 

 sult was obtained by the addition of liver mitochondria to ascites 

 tumor supernatant (Tiedemann and Born, 1958). 



However, while the above experiments resembled a Pasteur effect 

 in that the mitochondrial inhibition was only present aerobically, 

 addition of liver mitochondria to muscle supernatant inhibits anaer- 

 obically as well as aerobically (Sissakian and Pinus, 1958). Further- 

 more, when homologous mitochondria, i.e., mitochondria from the 

 same tissue, are used, such inhibition is absent altogether. This is 

 true for muscle (Sissakian and Pinus, 1958), Walker carcinoma 

 (Aisenberg et al., 1957), ascites tumor cells (Tiedemann and Born, 

 1958 ) , and brain ( Cremer, 1960 ) . The latter investigator also found 

 that liver mitochondria inhibited anaerobic CO2 release from bicar- 

 bonate buffer; he attributed this to decreased lactic acid formation 

 and hence a glycolysis inhibition. 



Here an additional difficulty arises. The classic way of measuring 

 glycolysis by a Qcoo ( though not as prevalent nowadays ) is extremely 

 deceiving, since hexokinase is a hvdrogen ion liberating reaction. 

 The apparent discrepancy between Aisenberg's results and Cremer's 

 result may well be non-existent. Sachsenmaier (1960) found an 

 inhibition as described by Cremer. He, however, traced the effect 

 to the action of mitochondrial DPN-ase, in contrast to the conclu- 

 sions by Cremer who favored the ATP-ase activity as the explana- 

 tion of the effect of liver mitochondria. 



The lack of effect of homologous mitochondria is, however, a se- 



