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The Inhibition of Respiration by Glucose, Fructose, and Mannose in the Ehrlich Mouse Ascites Tumor^*

Myron Brin and Ralph W. McKee

( Cancer Research Institute, New England Deaconess Hospital, and Department of Biological Chemistry, Harvard Medical School, Boston, Mass.)

1. The respiration of the mouse ascites tumor was inhibited equally by glucose, fructose, and mannose at concentrations above 30 mg. per cent at a phosphate concentration of 20 mM/l. The inhibition was released in 2–3 hours, after which interval respiration was accelerated. Below 30 mg. per cent, respiration was stimulated. Studies of aerobic glycolysis demonstrated that the glucose had disappeared and that the appearance of lactate was maximal just before the release of the inhibition.

2. These hexoses inhibited not only endogenous respiration but also that obtained from the oxidation of L(+)-lactate and other metabolites. L(+)-lactate was oxidized by the tumor in preference to D(-)-lactate.

3. Attempts to prevent the inhibition by the addition of accelerators, coenzymes, and various metabolites were unsuccessful. Raising the concentration of inorganic phosphate to 55 mM/l, however, reduced the inhibition markedly. These observations are discussed in terms of a competition by the glycolysis enzymes with the oxidative enzymes for phosphate.

^* This work was carried out under U.S. Atomic Energy Contract, AT(30-1)-901, with the New England Deaconess Hospital.

Present address: Thorndike Memorial Laboratory, Boston City Hospital, and the Dept. of Biological Chemistry, Harvard Medical School, Boston, Mass.

Present address: Dept. of Physiological Chemistry, University of California Medical Center, Los Angeles 24, Calif.

Received 12/16/55.

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