Tri-Calciphor (16,16-dimethyl-15-dehydroprostagalndin B1 trimer)-mediated mitochondrial Ca2+ movements: modulation by phosphate |
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Authors: | Salvador Uribe Thomas M. Devlin |
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Affiliation: | 1. Department of Biological Chemistry, Hahnemann University, School of Medicine, Mail Stop 411, Broad and Vine Streets, Philadelphia, PA 19102-1192 USA;2. Instituto de Fisiologia Celular, UNAM, Apdo. Postal 70-600, Mexico DF Mexico |
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Abstract: | 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, phopsphate and Mg2+ added together, and partially inhibited with phosphate plus either ATP or Mg2+. Between 0 and 7 μM 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. |
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Keywords: | Ischemia Tri-Calciphor Mitochondrion Calcium ionophore Calcium Corresponding author. Fax: + 1 (215) 2465836. |
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