Control of the pyridine nucleotide-linked Ca release from mitochondria by respiratory substrates |
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Authors: | Vladimir Gogvadze Matthias Schweizer Christoph Richter |
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Affiliation: | Laboratory of Biochemistry I, Swiss Federal Institute of Technology (ETH), Zürich, Switzerland |
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Abstract: | Oxidation of mitochondrial pyridine nucleotides followed by their hydrolysis promotes Ca2+ release from intact liver mitochondria. In most of the previous studies oxidation was achieved with pro-oxidants which were added to mitochondria respiring on succinate in the presence of rotenone, a site I-specific inhibitor of the respiratory chain. Here we investigate pro-oxidant dependent and independent Ca2+ release from mitochondria when respiration is supported either by the NAD+-linked substrate β-hydroxybutyrate, or by succinate. In the presence, as well as in the absence, of the pro-oxidant t-butylhydroperoxide mitochondria retain Ca2+ much better with succinate than with β-hydroxybutyrate, as respiratory substrate. When Ca2+ release is induced by t-butylhydroperoxide succinate-supported Ca2+ retention is impeded by rotenone. Ca2+ release (pro-oxidant dependent or independent) is paralleled by oxidation and hydrolysis of intramitochondrial pyridine nucleotides, and Ca2+ retention is paralleled by reduction of pyridine nucleotides. It is concluded that the pyridine nucleotide-linked Ca2+ release from mitochondria can be controlled by respiratory substrates which regulate the intramitochondrial hydrolysis of oxidized pyridine nucleotides. |
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Keywords: | Abbreviations: CSA, cyclosporine A EGTA, ethylene glycol bis((β-aminoethylether)-N,N,N′,N′-tetraacetic acid HEPES, 4-(2hydroxyethyl)-1-piperazine ethanesulfonic acid tbh, t-butylhydrope roxide Tris, tris(hydroxymethyl)aminomethane |
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