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Ca2+ release from energetically coupled tumor mitochondria.

C R Fleschner·A P Martin·M L Vorbeck·J R Darnold·J W Long
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Abstract

A Na+/Ca2+ exchange activity for Ca2+ efflux has been identified in isolated Ehrlich ascites tumor mitochondria. Further, under conditions favoring cycling of Ca2+ across the mitochondrial inner membrane, extramitochondrial [Ca2+] also was shown to be Na+-dependent. The Na+/Ca2+ exchange showed sigmoidal kinetics with a mean (+/-SD) [Na+] required for half maximal stimulation of Ca2+ efflux of 8.4 +/- 3.8 mM and a Hill coefficient of 1.6. Na+/Ca2+ exchange was very sensitive to inhibition by the Ca2+ antagonist diltiazem (56% inhibition at 7.5 nmoles X mg protein-1) whereas a number of other compounds, including verapamil, nupercaine, and trifluoperazine were less effective in inhibiting Ca2+ efflux. These data demonstrate for the first time the presence of a pathway in tumor mitochondria for unidirectional Ca2+ efflux induced by Na+, and provide a mechanism for regulation of tumor intra- and extramitochondrial [Ca2+]. Results of the present study support the need for further study of intracellular Na+ and its role in regulation of Ca2+ homeostasis in tumor cells.

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AnimalsCalciumCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneCarcinoma, Ehrlich TumorCell LineDibucaineMaleMiceMitochondriaSodiumTrifluoperazineVerapamilJournal ArticleResearch Support, U.S. Gov't, P.H.S.

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C R Fleschner, A P Martin, M L Vorbeck, J R Darnold, J W Long. 1983-09-15. Ca2+ release from energetically coupled tumor mitochondria.. https://doi.org/10.1016/s0006-291x(83)80162-4

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