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Catabolism of 2-deoxyglucose by Phagocytic Leukocytes in the Presence of 12-O-tetradecanoyl Phorbol-13-acetate

Peter Zabos, David Kyner, Naomi Mendelsohn, Carol Schreiber, Samuel Waxman, Judith Christman and George Acs
Proceedings of the National Academy of Sciences of the United States of America
Vol. 75, No. 11 (Nov., 1978), pp. 5422-5426
Stable URL: http://www.jstor.org/stable/68643
Page Count: 5
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Catabolism of 2-deoxyglucose by Phagocytic Leukocytes in the Presence of 12-O-tetradecanoyl Phorbol-13-acetate
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Abstract

We have found that phagocytic leukocytes exposed to the tumor-promoting agent, 12-O-tetradecanoyl phorbol-13-acetate, efficiently release carbon-1 of 2-deoxyglucose in the form of CO2 with concurrent intracellular accumulation of a phosphorylated 5-carbon intermediate. In the absence of 12-O-tetradecanoyl phorbol-13-acetate, these cells release barely detectable amounts of CO2 from 2-deoxyglucose. 12-O-Tetradecanoyl phorbol-13-acetate, at a concentration of 1 ng/ml, has an immediate effect on CO2 release, which is temperature-dependent and linear with time and cell number. The ability of a number of phorbol ester-like compounds to enhance this catabolic pathway for 2-deoxyglucose correlates with their ability to act as tumor promotors and inflammatory agents. Although this effect of phorbol esters appears to be restricted to granulocytes, monocytes, and macrophages, the possibility arises that other mammalian cells are capable of catabolizing or can be induced to catabolize 2-deoxyglucose. Thus, 2-deoxyglucose decarboxylation should be considered whenever this analog of mannose and glucose is used as an indicator for sugar transport, especially when pharmacodynamic agents are present.

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