Glycolytic Control Mechanisms

Abstract

Abstract Sections of the main electric organ of Electrophorus were stimulated electrically to elicit a discharge, and slices were cut by a rapid sampling guillotine during and after different times of discharge. Kinetic measurements of adenine nucleotides, creatine phosphate, and inorganic phosphate showed that a disappearance of creatine phosphate occurred within a few seconds of the onset of discharge. The levels of ATP were maintained approximately constant by the high activity of creatine phosphokinase, and marked increases of ADP and AMP were not observed until after the end of a 60-sec discharge period, when the creatine phosphate reserves were depleted. Phosphofructokinase activity, as depicted by changes in the phosphofructokinase mass action ratio [fructose-di-P x ADP/fructose-6-P x ATP], increased during discharge but showed a further large but transient increase during recovery, especially after discharge times greater than 40 sec. The initial activation of phosphofructokinase was caused by the early rise of inorganic phosphate, but thereafter the change of the phosphofructokinase mass action ratio followed closely the changes of ADP and AMP. The results show that the duration and magnitude of the increased glycolytic flux after electric discharge of the organ are controlled by the rapid activation and deactivation of phosphofructokinase, which is turned on and off by feedback from the energy-utilizing reactions of the sodium pump.