Treatment of Breast Tumor Cells In Vitro with the Mitochondrial Membrane Potential Dissipater Valinomycin Increases 18F-FDG Incorporation
Tim A.D. Smith1 and
Morgan G. Blaylock2
1 John Mallard PET Centre, School of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, Scotland; and 2 Institute of Medical Sciences, School of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, Scotland
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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.
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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).
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FIGURE 3. Initial rate of OMG uptake by cells treated for 30 min with valinomycin (n = 7, treated and controls).
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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).
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Copyright © 2007 by the Society of Nuclear Medicine.
