Rapid and extensive release of Ca2+ from energized mitochondria induced by EGTA.
A novel mitochondrial Ca2+ release phenomenon is reported. When rat liver mitochondria (oxidizing succinate) are allowed to accumulate Ca2+ in excess of 40 nmol/mg protein and are then treated with excess EGTA, a fraction of the accumulated cation is rapidly (approximately 1 nmol/s/mg protein) released. The size of the released fraction is an apparent function of the extramitochondrial Ca2+ concentration at the time of EGTA addition and can attain a maximal value of approximately 30 nmol/mg protein. Release is inhibited by ruthenium red (I50 approximately 50 pmol/mg protein) and is not dependent on the presence of Na+ or K+ in the medium. During the period of rapid release, O2 consumption is inhibited, membrane potential increases, and apparent H+ accumulation occurs at a ratio of approximately 2H+ per Ca2+ released. It is proposed that this chelator-induced Ca2+ release occurs by reverse uniport with H+ back diffusion to the matrix space providing charge movement compensation.
Riley
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Pfeiffer
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D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004533:Egtazic Acid / Q000494:pharmacology*; D005026:Ethylene Glycols / Q000494:pharmacology*; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012430:Ruthenium Red / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology
D005026:Ethylene Glycols; D012430:Ruthenium Red; D004533:Egtazic Acid; D012964:Sodium; D011188:Potassium; D002118:Calcium