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Novel oxaloacetate effect on mitochondrial Ca 2+ movement
Author(s) -
Leikin Yuri N.,
Zharova Tatjana V.,
Tjulina Olga V.
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)80292-3
Subject(s) - citrate synthase , arsenite , chemistry , mitochondrion , biochemistry , calcium , biophysics , membrane potential , phosphoenolpyruvate carboxykinase , biology , enzyme , organic chemistry , arsenic
Mitochondrial Ca 2+ movement was investigated in the presence of oxaloacetate, which is widely known as a ‘Ca 2+ ‐releasing’ agent [1978, Proc. Natl. Acad. Sci. USA 75, 1690‐1694]. It is demonstrated that rat liver mitochondria are capable of net Ca 2+ accumulation from the oxaloacetate supplemented assay mixture. Both the membrane energization and the cation uniport at the expense of oxaloacetate are shown to be specifically blocked by either arsenite or ammonium chloride. With respiratory inhibitors present, ADP is shown to be a prerequisite for a high Ca 2+ capacity, which can be alternatively enlarged with a concomitant loss of the arsenite effect by an addition of an NADP + ‐specific reductant (isocitrate). Arsenite‐sensitive production of NADPH is observed, thus suggesting coupling between pyridine nucleotide transhydrogenation and the cation uniport in mitochondria. The role of such a coupling mechanism in the uniporter‐mediated Ca 2+ fluxes in mitochondria is discussed.