Novel oxaloacetate effect on mitochondrial Ca2+ movement

FEBS Letters

Zharova, Tatjana V.¹  Tjulina, Olga V.¹  Leikin, Yuri N.¹ 

[1] Department of Biochemistry, School of Biology, Moscow State University, Moscow 119899, Russian Federation

关键词: Uniport of Ca2+;    Oxaloacetate;    NAD(P)-transhydrogenase (EC 1.6.1.1);    Mitochondria;    Rat liver;    OA;    oxaloacetate;    PN;    pyridine nucleotides;    RR;    ruthenium red;    FCCP;    carbonylcyanide-4-trifluoromethoxyphenylhydrazone;    HEPES;    4-(2-hydroxyethyl)piperazine-l-ethanesulfonic acid;   

DOI  :  10.1016/0014-5793(93)80292-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Mitochondrial Ca²⁺ movement was investigated in the presence of oxaloacetate, which is widely known as a ‘Ca²⁺-releasing’ agent [1978, Proc. Natl. Acad. Sci. USA 75, 1690-1694]. It is demonstrated that rat liver mitochondria are capable of net Ca²⁺ 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 Ca²⁺ 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 Ca²⁺ fluxes in mitochondria is discussed.

【 授权许可】

Unknown