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Intracellular Hydrogen Transport in Ehrlich Ascites Tumor Cells¹

Wenner-Gren Institute, University of Stockholm, Stockholm, Sweden

The high rate of aerobic glycolysis of Ehrlich ascites tumor cells has been attributed to an ineffective mechanism for the mitochondrial oxidation of reducing equivalents synthesized in the extramitochondrial compartment. The present experiments provide additional support for this conclusion. Inhibition of the tricarboxylic acid cycle with arsenite or fluorocitrate, or of the respiratory chain with rotenone or Amytal, restricted the metabolism of endogenous substrate with consequent inhibition of respiration. Addition of glucose or fructose to the inhibited system resulted in considerable lactate production, but failed to initiate respiration. However, in the presence of vitamin K₃, a shunt was established via DT diaphorase. Under these conditions, hexose addition led to a marked stimulation of respiration and diminished lactate production as a result of the transfer of hydrogen from extramitochondrial reduced pyridine nucleotides to the mitochondrial respiratory chain. Thus, hexose metabolism contributes reducing equivalents for mitochondrial oxidation in the presence of the "K₃-shunt," but not in its absence.

¹ This study was supported by USPHS Research Grant AM-02598 and by the Swedish Cancer Society. A part of this work has been reported in abstract form (13).

² Present address: Department of Medicine, Albert Einstein College of Medicine, New York, N. Y. Career Scientist of the Health Research Council of the City of New York (I-156) and recipient of USPHS Fellowship 7-F3-AM-7192-02.

Received 12/19/66. Accepted 4/ 5/67.