ROLE OF TRIPHOSPHOPYRIDINE NUCLEOTIDE 

 IN THE REGULATION OF GLYCOLYSIS IN A 

 CELL-FREE PREPARATION* 



Van R. Potter and Hermann Niemeyer f 



McArdle Memorial Laboratories for Cancer Research^ 

 University of Wisconsin, Madison 



Introduction 



It was previously reported that the addition of liver mito- 

 chondria to a glycolytic system consisting of the supernatant 

 fraction of brain and tumour homogenates decreases both the 

 glucose uptake and the lactic acid production (Aisenberg, 

 Reinafarje and Potter, 1957; Aisenberg and Potter, 1957). 

 These facts were interpreted as a Pasteur effect produced by 

 respiring mitochondria. The mitochondria obtained from 

 certain tumours did not exhibit such effect. A similar be- 

 haviour has been shown recently with mitochondria obtained 

 from Ehrlich ascites tumour (Tiedemann and Born, 1958). 

 Later on, it was demonstrated that the mechanisms concerned 

 with the oxidation of reduced triphosphopyridine nucleotide 

 (TPNH) are decreased or absent in Novikoff hepatoma, as 

 well as in some other tumours (Reinafarje and Potter, 1957). 



Since it is a well established fact that tumours possess a 

 characteristically high aerobic glycolysis (Warburg, 1930), it 

 seemed worthwhile to consider the possibility that oxidized 

 triphosphopyridine nucleotide (TPN) could exert a control on 

 glycolysis. 



* A portion of this work was presented at the meeting of the American 

 Association for Cancer Research, Philadelphia, April 11, 1958 (Niemeyer and 

 Potter, 1958). This work was supported in part by a grant (No. C-646) from 

 the National Cancer Institute, National Institutes of Health, United States 

 Public Health Service. 



t Fellow of the Rockefeller Foundation, on leave from Instituto de Quimica 

 Fisiologica y Patol6gica, Universidad de Chile, Santiago, Chile. 



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