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Intracellular Protein Breakdown in the L1210 Ascites Leukemia¹

Department of Experimental Therapeutics, Roswell Park Memorial Institute, Buffalo, New York 14203

The endogenous catabolism of the cell protein of the L1210 mouse ascites tumor has been estimated from its in vitro breakdown to free amino acid after pulse labeling in vivo with leucine-1-¹⁴C. Two general protein classes are distinguishable according to their breakdown: an unstable population representing one-fifteenth of the cell protein and with an average half-life of several hours, and the stable remaining protein with a uniform breakdown one-fifth the cumulative rate of the unstable class. Treated as a parameter of growth, the cumulative turnover of the unstable 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 breakdown rate. However, the selection of proteolyzable cellular substrates varies with the physiologic state of the cell. After treatment of the tumor with chemotherapeutic agents, breakdown is expanded to a broader spectrum of cellular substrates than are proteolyzed in growth.

¹ This work was supported by Grant CA-07777 from the National Cancer Institute, NIH, USPHS.

Received 6/23/66. Accepted 10/24/66.