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 insens
itive efflux mechanism. Extramitochondrial Na+ did not affect the rate
of Ca2+ efflux indicating that Na+/Ca2+ exchange mechanism is not inv
olved. Depolarization of inner mitochondrial membrane induced by the u
ncoupler 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 o
f 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+ transpo
rt mechanism might be intrinsic to the ADP/ATP carrier (AAC). Thus, th
e data indicate that sperm mitochondria contain a Ca2+ efflux mechanis
m operated via AAC and regulated by mitochondrial membrane potential a
nd by ADP concentration.