Abstract
This paper reports an investigation on calcium efflux mechanism in ram sperm mitochondria. Energized sperm mitochondria take up Ca2+ via the ruthenium-red sensitive uniporter, and possess a ruthenium-red insensitive efflux mechanism. Extramitochondrial Na+ did not affect the rate of Ca2+ efflux indicating that Na+/Ca2+ exchange mechanism is not involved. Depolarization of inner mitochondrial membrane induced by the uncoupler carbonylcyanide-p-trifluoromethoxyphenyl hydrazone (FCCP) or by the organomercurial SH-reagent mersalyl, causes high stimulation in Ca2+ efflux. This stimulated Ca2+ efflux determined in the presence of ruthenium-red and phosphate, is not inhibited by cyclosporin A (CSA), indicating that mitochondrial permeability transition pore (MTP) is not involved in this Ca2+ efflux mechanism. The stimulated Ca2+ efflux is inhibited by ADP or atractyloside suggesting that the Ca2+ transport mechanism might be intrinsic to the ADP/ATP carrier (AAC). Thus, the data indicate that sperm mitochondria contain a Ca2+ efflux mechanism operated via AAC and regulated by mitochondrial membrane potential and by ADP concentration.
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Schedule a callMore From: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
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