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A comparative study on proliferation, macromolecular synthesis and energy metabolism of in vitro-grown ehrlich ascites tumor cells in the presence of glucosone, galactosone and methylglyoxal

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Summary

  1. 1.

    Proliferation of in vitro grown Ehrlich ascites tumor cells is completely inhibited by 0.2–0.4 mM methylglyoxal and 1–2mM glucosone or galactosone without severely affecting viability (dye exclusion test); no phase-specific arrest of cell growth is observed.

  2. 2.

    Incorporation of [14C] thymidine into the acid-insoluble fraction of the cells decreases within a few minutes to less than 50% of that in controls in the presence of 0.4 mM methylglyoxal, and 2 mM glucosone or galactosone causes a comparable inhibition of DNA synthesis after 2 h or 4 h, respectively.

  3. 3.

    The action of 0.4 mM methylglyoxal inhibits incorporation of [14C] leucine within a few minutes by more than 70%, while 2 mM glucosone and galactosone are significantly less effective (50%–60% inhibition after 12 h).

  4. 4.

    While methylglyoxal and galactosone do not severely affect lactate production of the cells, 2 mM glucosone reduces glycolysis by 60%–70%; ATP/ADP ratios did not fall below 3.5 in the presence of the inhibitors (controls 4–6).

  5. 5.

    It is suggested that the reaction potentialities of the oxaldehyde function of the inhibitors play an important role in their growth-inhibitory acitivity, besides exerting a specific effect on hexokinase (glucosone) and UTP-trapping activity.

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Dedicated to Prof. H. Witzel on the occasion of his 60th birthday

This work was supported by the Deutsche Forschungsgemeinschaft, Sonderforschungsbereich “Zellenergetik und Zelldifferenzierung”

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Reiffen, K.A., Schneider, F. A comparative study on proliferation, macromolecular synthesis and energy metabolism of in vitro-grown ehrlich ascites tumor cells in the presence of glucosone, galactosone and methylglyoxal. J Cancer Res Clin Oncol 107, 206–210 (1984). https://doi.org/10.1007/BF01032608

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  • DOI: https://doi.org/10.1007/BF01032608

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