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“Portable Battery: What is the Worst-Case Soluion” by Alexander Ermolosov University of CambridgeInhibition of the Na+/H+ exchanger (NHE) rescues valinomycin-induced apoptosis in renal cell cancer cells.
We studied whether apoptosis induced by hypoxia and/or valinomycin in renal cell cancer (RCC) cells was associated with increased permeability of the cell membrane to sodium. In addition, we determined whether inhibiting the Na+/H+ exchanger (NHE) could protect cells from this toxicity. The human RCC cell line ACHN was exposed to hypoxia and/or valinomycin. NHE-activity, cell volume and cell viability were assessed, using pH microelectrodes, a method allowing continuous recording of cell volume changes and a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, respectively. Whereas valinomycin and hypoxia alone induced apoptosis, co-application resulted in a mixed population of apoptotic and necrotic cells. The apoptotic response depended on time and was not accompanied by an increase in cell volume. Inhibiting NHE by monensin fully protected the cells against valinomycin-induced apoptosis. Although inhibition of NHE did not protect the cells against hypoxia-induced apoptosis, it increased the number of necrotic cells. Exposure of RCC cells to valinomycin leads to a state of cellular stress. We suggest that this results in increased cell volume and concomitant release of endogenous apoptotic factors. We further propose that the effects of valinomycin are similar to those observed in chronic heart failure, being related to a final common pathway involving increased permeability of the cell membrane to sodium.
106 N.H. 408 (1965)
JOAN JONES ET AL.
v.
ALBER
3e33713323

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