282 G. ASHWELL, Z. DISCHE VOL. 4 (1950) 



of 75-150 y/ml per hour. The O2 consumption increases at the same time considerably 

 by 13-50% in 4 hours. At the same time an intensive aerobic glycolysis and sometimes 

 esterification of inorganic P to difficultly hydrolyzable esters is observed. Up to 260 

 y/ml of lactic is produced in 4 hours. The rate of O2 consumption during the first hour 

 is different from the rate in the following 3 hours during which it remains almost con- 

 stant. The rate of glycolysis is in general smaller during the first hour than later. If 

 we assume that the additional 0^ consumption in presence of glucose is due to the total 

 oxidation of the latter and calculate the total breakdown of glucose by oxidation and 

 glycolysis the latter turns out to be considerably smaller than the amount of glucose 

 which really disappeared. The R.Q. of the additional respiration due to glucose is only 

 about 0.7 (Table VI). The discrepancy between the observed values and those calculated 

 for glucose which disappears indicates that only one part of it is completely oxidized 

 while another part is oxidized either to phosphogluconic or pyruvic acid. 



3. The coupling between aerobic glycolysis and respiration 



The glycolysis of the hemolysate is obligatorily aerobic and disappears almost 

 completely when the oxidation processes in the hemolysate are suppressed either by 

 inhibitors or by elimination of O^. Thus NaCN at M/250 almost completely suppresses 

 the glycolysis and 90% of the total O2 consumption. (Table I) Further increase of the 

 concentration does not have any significant effect. The small residual glycolysis amounts 

 to only a few per cent of the total and is probably due to the leucocytes which were 

 not removed. The leucocytes which are siphoned off in the beginning of the blood wash- 

 ing display in fact a powerful anaerobic glycolysis which is partly suppressed in aero- 

 biosis. That the effect of cyanide on glycolysis is due to the blocking of respiration could 

 be shown in experiments in which O^ was removed from the hemolysate. These were 

 carried out in the following way. 4 ml of the hemolysate + 0.8 ml of 0.3% glucose 

 solution were pipetted into a 500 ml flask which was closed by a ground stopper with 

 stopcock. The flask was weighed and then evacuated first with a water pump. When 

 the foaming of the fluid became too intense the evacuation was interrupted until the 

 foam broke down and the evacuation then resumed until no more gas escaped. The 

 evacuation was continued with the oil pump until a vacuum of about i mm Hg was 

 obtained. The flask was then weighed again to determine the loss in water. The hemo- 

 lysate was kept in vacuo for 4 hours at room temperature and then the flask opened, 

 the evaporated water replaced and the hemolysate deproteinized simultaneously with 

 a control, which stayed during the same period in presence of oxygen and one 

 to which NaCN M/500 was added. The determination of lactic acid showed that the 

 glycolysis was suppressed in the sample in vacuo, though not quite as far as in the 

 sample with NaCN. 



While suppression of the Og consumption inhibits the glycolysis in our hemolysate 

 any increase of Og consumption after addition of pyruvate, citrate and dicarboxylic 

 acids of the Krebs cycle is accompanied by a strong increase of glycolysis (Table II). 

 If the final dilution of the hemolysate is no more than the threefold of the original 

 volume of the suspension, a-ketoglutarate is most effective, with succinate and fumarate 

 following, and pyruvate the least effective. It was found for the succinate that the 

 promoting effect on glycolysis increases with the concentration, as also does the Og 

 consumption. 

 References p. 2g2. 



