Novel oxaloacetate effect on mitochondrial Ca2+ movement.
Mitochondrial Ca2+ 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 mitochondrial 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.
Leikin
Y N
YN
Department of Biochemistry, School of Biology, Moscow State University, Russian Federation.
Zharova
T V
TV
Tjulina
O V
OV
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D066298:In Vitro Techniques; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D009243:NAD / Q000378:metabolism; D009249:NADP / Q000378:metabolism; D009250:NADP Transhydrogenases / Q000378:metabolism; D010071:Oxaloacetates / Q000494:pharmacology*; D051381:Rats
D010071:Oxaloacetates; D009243:NAD; D009249:NADP; D009250:NADP Transhydrogenases; D002118:Calcium