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Release from the Crabtree effect by hypoxic cell radiosensitizers.

I Mustea, A Bara

    British Journal of Cancer
    |August 1, 1979
    PubMed
    Summary

    Glucose induces the Crabtree effect in Ehrlich ascites tumor cells, inhibiting oxygen consumption. Hypoxic cell radiosensitizers like misonidazole and NDPP reversed this effect, stimulating oxygen utilization.

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    Area of Science:

    • Cellular metabolism
    • Cancer research
    • Biochemistry

    Background:

    • The Crabtree effect describes increased glycolysis despite oxygen availability in certain cells.
    • Tumor cells often exhibit the Crabtree effect, impacting their metabolic profile.
    • Understanding metabolic adaptations is crucial for cancer therapy.

    Purpose of the Study:

    • To investigate the impact of glucose on oxygen consumption in Ehrlich ascites tumor cells.
    • To evaluate the effect of hypoxic cell radiosensitizers (misonidazole, NDPP) on cellular respiration in the presence and absence of glucose.
    • To determine if these radiosensitizers can overcome the Crabtree effect.

    Main Methods:

    • Measuring oxygen consumption of Ehrlich ascites tumor cells in media with and without glucose.
    • Comparing the effects of varying concentrations of misonidazole and NDPP on oxygen consumption.
    • Analyzing the percentage of oxygen consumption inhibition relative to glucose presence.

    Main Results:

    • Glucose induced a significant Crabtree effect in Ehrlich ascites tumor cells, inhibiting oxygen consumption by 38-45%.
    • Misonidazole (5-20mM) and NDPP (0.5mM) demonstrated a stimulatory effect on oxygen consumption in glucose-containing media.
    • These radiosensitizers appeared to release cells from the Crabtree effect, increasing oxygen utilization.

    Conclusions:

    • Glucose triggers the Crabtree effect in Ehrlich ascites tumor cells, leading to suppressed oxygen consumption.
    • Hypoxic cell radiosensitizers misonidazole and NDPP can counteract the Crabtree effect by enhancing oxygen utilization.
    • These findings suggest a potential metabolic vulnerability in tumor cells that can be targeted by radiosensitizers.

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