TRI-CALCIPHOR (16,16-DIMETHYL-15-DEHYDROPROSTAGLANDIN B-1 TRIMER)-MEDIATED MITOCHONDRIAL CA2- MODULATION BY PHOSPHATE( MOVEMENTS )

The trimeric derivative of 16,16-dimethyl-15-dehydroprostaglandin B-1 (termed tri-Calciphor), which protects tissues against ischemic damage , induced Ca2+ efflux and swelling in mitochondria in the absence of p hosphate, Mg2+ and ATP. When glutamate/malate rather than succinate wa s the substrate, higher tri-Calciphor concentrations were required for the ionophoretic activity. Ca2+ efflux and mitochondrial swelling ind uced by tri-Calciphor were completely inhibited by ATP, phosphate and Mg2+ added together, and partially inhibited with phosphate plus eithe r ATP or Mg2+. Between 0 and 7 mu M added Ca2+ and in the presence of phosphate, ATP and Mg2+, tri-Calciphor stimulated the uptake of Ca2+ b y mitochondria and increased the efficiency of buffering of extramitoc hondrial Ca2+. Thus, depending on the assay conditions, two different effects involving Ca2+ movements and mitochondria are observed with tr i-Calciphor.