Journal article
Tri-Calciphor (16,16-dimethyl-15-dehydroprostagalndin B 1 trimer)-mediated mitochondrial Ca 2+ movements: modulation by phosphate
Biochimica et biophysica acta. Molecular basis of disease, v 1225(2)
1994
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Abstract
The trimeric derivative of 16,16-dimethyl-15-dehydroprostaglandin B
1 (termed tri-Calciphor), which protects tissues against ischemic damage, induced Ca
2+ efflux and swelling in mitochondria in the absence of phosphate, Mg
2+ and ATP. When glutamate/malate rather than succinate was the substrate, higher tri-Calciphor concentrations were required for the ionophoretic activity. Ca
2+ efflux and mitochondrial swelling induced by tri-Calciphor were completely inhibited by ATP, phopsphate and Mg
2+ added together, and partially inhibited with phosphate plus either ATP or Mg
2+. Between 0 and 7 μM added Ca
2+ and in the presence of phosphate, ATP and Mg
2+, tri-Calciphor stimulated the uptake of Ca
2+ by mitochondria and increased the efficiency of buffering of extramitochondrial Ca
2+. Thus depending on the assay conditions, two different effects involving Ca
2+ movements and mitochondria are observed with tri-Calciphor.
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Details
- Title
- Tri-Calciphor (16,16-dimethyl-15-dehydroprostagalndin B 1 trimer)-mediated mitochondrial Ca 2+ movements: modulation by phosphate
- Creators
- Salvador Uribe - Hahnemann University HospitalThomas M. Devlin - Hahnemann University Hospital
- Publication Details
- Biochimica et biophysica acta. Molecular basis of disease, v 1225(2)
- Publisher
- Elsevier
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Biochemistry and Molecular Biology
- Web of Science ID
- WOS:A1994MY08200004
- Scopus ID
- 2-s2.0-0028177970
- Other Identifier
- 991019184068304721
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- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Biochemistry & Molecular Biology
- Biophysics
- Cell Biology