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Glycolysis by Sarcoma 180 of Mice Treated with 6-Mercaptopurine

II. Conditions Determining the Formation of Pyruvate from 3-Phosphoglycerate^*

Paul J. Fodor and H. Christine Reilly

( Division of Enzymology and Metabolism and the Division of Experimental Chemotherapy, Sloan-Kettering Institute for Cancer Research; and the Sloan-Kettering Division, Cornell University Graduate School of Medical Sciences, New York, New York)

The formation of pyruvate from 3-D-phosphoglycerate by Sarcoma 180 homogenates from mice treated with 6-mercaptopurine was investigated under aerobic and anaerobic conditions. The anaerobic conditions required the saturation of both media and homogenates with a gas mixture consisting of 95 per cent N₂ and 5 per cent CO₂, preceding the start of the reaction. The sharp drop in pyruvate output of the gassed homogenates was correlated with the inactivation of enolase. Pyruvate formation was restored by reinforcement of these homogenates with crystalline muscle enolase, the activity of which remained unchanged after treatment with N₂/CO₂. In the course of the saturation of the homogenates with this gas mixture a drop from their initial pH of 7.1 ± 0.1 to 6.2 ± 0.1 was observed. The inactivation of enolase was not specific for CO₂ but could be duplicated in the pH range of 6.1–6.4 by acetate buffer but not by phosphate buffer. Moreover, the presence of phosphate buffer of pH 6.2 protected the enolase from inactivation by treatment with N₂/CO₂ or from inactivation by acetate buffer. In contrast, saturation with N₂/CO₂ or acidification to pH 6.2 with acetate buffer caused only minor decreases of the enolase activity in tumor homogenates of the nontreated control animals, and saturation with this gas mixture did not change their pyruvate output. The enolase in the tumor homogenates of the 6-mercaptopurine-treated hosts showed a considerably greater heat lability than that in the tumor homogenates from the control animals. The significance of these results has been discussed.

^* This work has been supported in part by American Cancer Society Grants P-163 and P-164, by a contract, SA-43-ph-2445, from the Cancer Chemotherapy National Service Center, and by Public Health Service Grant CA-03192-08.

Dr. Fodor died on October 7, 1964.

Received 6/ 8/64.