Intracellular protein breakdown in the L1210 ascites leukemia.

The endogenous catabolism of the cell protein of the L1210 mouse ascites tumor has been estimated from its in vitro break down to free amino acid after pulse labeling in vivowith leucine1-14C.Two general protein classes are distinguishable according to their breakdown: an unstable population representing onefifteenth of the cell protein and with an average half-life of several hours, and the stable remaining protein with a uniform break down one-fifth the cumulative rate of the unstable class. Treated as a parameter of growth, the cumulative turnover of the un stable class requires the expenditure of 5% of the biosynthetic capacity of the cell per hour, and comprises one-third of the total cellular protein turnover of 1.5%/hour. None of a variety of inhibitory agents administered in vivo or in vitro selectively stimulates or inhibits the cumulative break down rate. However, the selection of proteolyzable cellular sub strates varies with the physiologic state of the cell. After treat ment of the tumor with chemotherai)eutic agents, breakdown is expanded to a broader spectrum of cellular substrates than are proteolyzed in growth.