Journal
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 386, Issue 2, Pages 251-260Publisher
ELSEVIER SCIENCE INC
DOI: 10.1006/abbi.2000.2201
Keywords
adenylate kinase; cyclosporin A; dibucaine; propranolol; membrane potentials; mitochondrial swelling
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Funding
- NIGMS NIH HHS [GM57429] Funding Source: Medline
- NINDS NIH HHS [NS34152] Funding Source: Medline
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This study tested the hypothesis that mitochondrial precursor targeting peptides can elicit the release of cytochrome c from both liver and brain mitochondria by a mechanism distinct from that mediated by the classical, Ca2+-activated permeability transition pore. Human cytochrome oxidase subunit IV signal peptide (hCOXIV(1.22)) at concentrations from 15 to 100 muM induced swelling, a decrease in membrane potential, and cytochrome c release in both types of mitochondria, Although cyclosporin A and bongkrekic acid were without effect, dibucaine, propanolol, dextran, and the uncoupler FCCP were each able to inhibit signal peptide-induced swelling and cytochrome c release. Adenylate kinase was coreleased with cytochrome c, arguing against a signal peptide-induced cytochrome c-specific pathway of efflux across the outer membrane. Taken together, the data indicate that a human mitochondrial signal peptide can evoke the release of cytochrome c from both liver and brain mitochondria by a unique permeability transition that differs in several characteristics from the classical mitochondrial permeability transition. (C) 2001 Academic Press.
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