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The elaboration of high energy phosphate bonds has assumed a crucial role (1) in the energy conversions associated with the maintenance of biological systems. The transfer of this bound energy is mediated principally through the turnover of adenosinetriphosphate 1 which is derived either from aerobic respiration or by glycolysis in animal tissues when integrated enzyme systems catalyze the esterification of adenine nucleotide acceptors with inorganic phosphate. The bulk of the evidence for this concept is derived from studies on tissue dispersions or "cell-free homogenates" which are essentially suspensions of cellular particles obtained by mashing or grinding tissues until few intact cells remain. Several workers have shown that the metabolic activity of mashed tissue is brief but can be slightly prolonged by procedures which generate and conserve the high energy phosphorylated intermediates. It is not oxidation alone but the extent of accompanying oxidative phosphorylation and the utilization of phosphorylation energy which determine the structural and metabolic perpetuation of the constituents of tissue dispersions (2). Under such severe treatment as maceration it is not very remarkable, as Barron, Ardao, and He~ron (3) so aptly demonstrate in their studies, that the metabolic patterns and pathways of disrupted and whole cells are very different.It is pertinent, therefore, to inquire into the circumstances which contribute to alterations in metabolism when cells are ruptured. The injurious effect of breaking cells has been attributed to the dissolution of organization and the consequent release of autolytic enzymes normally segregated in the cell among the different discrete cellular particles. A rapid depletion of ,-~P reserves en-

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