Tri-Calciphor (16,16-dimethyl-15-dehydroprostaglandin B1 trimer)-mediated mitochondrial Ca2+ movements: modulation by phosphate.
The trimeric derivative of 16,16-dimethyl-15-dehydroprostaglandin B1 (termed tri-Calciphor), which protects tissues against ischemic damage, induced Ca2+ efflux and swelling in mitochondria in the absence of phosphate, Mg2+ and ATP. When glutamate/malate rather than succinate was the substrate, higher tri-Calciphor concentrations were required for the ionophoretic activity. Ca2+ efflux and mitochondrial swelling induced by tri-Calciphor were completely inhibited by ATP, phosphate and Mg2+ added together, and partially inhibited with phosphate plus either ATP or Mg2+. Between 0 and 7 microM added Ca2+ and in the presence of phosphate, ATP and Mg2+, tri-Calciphor stimulated the uptake of Ca2+ by mitochondria and increased the efficiency of buffering of extramitochondrial Ca2+. Thus, depending on the assay conditions, two different effects involving Ca2+ movements and mitochondria are observed with tri-Calciphor.
Uribe
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Department of Biological Chemistry, Hahnemann University, School of Medicine, Philadelphia, PA 19102-1192.
Devlin
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D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects* / Q000378:metabolism; D009840:Oligomycins; D010710:Phosphates / Q000494:pharmacology*; D011456:Prostaglandins B / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013386:Succinates / Q000378:metabolism; D019802:Succinic Acid
C052137:16,16-dimethyl-15-dehydroprostaglandin B1 trimer; D005971:Glutamates; D009840:Oligomycins; D010710:Phosphates; D011456:Prostaglandins B; D013386:Succinates; D018698:Glutamic Acid; D000255:Adenosine Triphosphate; D019802:Succinic Acid; D008274:Magnesium; D002118:Calcium