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Treatment of Breast Tumor Cells In Vitro with the Mitochondrial Membrane Potential Dissipater Valinomycin Increases 18F-FDG Incorporation

Tim A.D. Smith and Morgan G. Blaylock
Journal of Nuclear Medicine August 2007, 48 (8) 1308-1312; DOI: https://doi.org/10.2967/jnumed.107.041665

Article Figures & Data

Figures

  • FIGURE 1. 
    FIGURE 1. 

    Fluorescence of MCF-7 control cells (A) and valinomycin-treated cells (30 min) (B) incubated with mitochondrial membrane potential probe JC-1. x- and y-axes are green and red fluorescence, respectively. Valinomycin-treated cells show loss of red fluorescence (loss of membrane potential–dependent accumulation in mitochondria) indicative of mitochondrial membrane depolarization.

  • FIGURE 2. 
    FIGURE 2. 

    18F-FDG incorporation by control MCF-7 cells (n = 7) treated for 30 min (n = 7) and 3.5 h (n = 4) with valinomycin (% control).

  • FIGURE 3. 
    FIGURE 3. 

    Initial rate of OMG uptake by cells treated for 30 min with valinomycin (n = 7, treated and controls).

  • FIGURE 4. 
    FIGURE 4. 

    Hexokinase activity total (% control) and mitochondrial hexokinase (% total activity by cell extracts treated with valinomycin for 30 min) (n = 6, treated and control).

Tables

  • TABLE 1

    ATP Content and Lactate Production by Control and Treated MCF-7 Cells

    MCF-7 cell groupATP*Lactate†
    Control15.4 ± 4.63.4 ± 0.98
    Valinomycin-treated (30 min)19 ± 5.85.4 ± 0.95

    • ↵* μg/mg of protein; n = 15 for both.

    • ↵† μmol formed/mg of protein/15 min; n = 8 for both.

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