ArticleJournal of bioenergetics and biomembranes2007
Mitochondrial Ca2+ cycle mediated by the palmitate-activated cyclosporin A-insensitive pore.
Article in Journal of bioenergetics and biomembranes, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Bile Acids as Inducers of Protonophore and Ionophore Permeability of Biological and Artificial Membranes.Membranes · 2023Review
- The Short-Term Opening of Cyclosporin A-Independent Palmitate/SrMembranes · 2022Article
- Review
- Palmitate Stimulates the Epithelial Sodium Channel by Elevating Intracellular Calcium, Reactive Oxygen Species, and Phosphoinositide 3-Kinase Activity.Oxidative medicine and cellular longevity · 2018Article
- Palmitic acid induces the opening of a Ca2+-dependent pore in the plasma membrane of red blood cells: the possible role of the pore in erythrocyte lysis.The Journal of membrane biology · 2010Article
- Physiological aspects of the mitochondrial cyclosporin A-insensitive palmitate/Ca2+-induced pore: tissue specificity, age profile and dependence on the animal's adaptation to hypoxia.Journal of bioenergetics and biomembranes · 2009Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Earlier we found that in isolated rat liver mitochondria the reversible opening of the mitochondrial cyclosporin A-insensitive pore induced by low concentrations of palmitic acid (Pal) plus Ca(2+) results in the brief loss of Deltapsi [Mironova et al., J Bioenerg Biomembr (2004), 36:171-178]. Now we report that Pal and Ca(2+), increased to 30 and 70 nmol/mg protein respectively, induce a stable and prolonged (10 min) partial depolarization of the mitochondrial membrane, the release of Ca(2+) and the swelling of mitochondria. Inhibitors of the Ca(2+) uniporter, ruthenium red and La(3+), as well as EGTA added in 10 min after the Pal/Ca(2+)-activated pore opening, prevent the release of Ca(2+) and repolarize the membrane to initial level. Similar effects can be observed in the absence of exogeneous Pal, upon mitochondria accumulating high [Sr(2+)], which leads to the activation of phospholipase A(2) and appearance of endogenous fatty acids. The paper proposes a new model of the mitochondrial Ca(2+) cycle, in which Ca(2+) uptake is mediated by the Ca(2+) uniporter and Ca(2+) efflux occurs via a short-living Pal/Ca(2+)-activated pore.
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