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Vol. 12, Issue 1, 63-71, January 2001
*Instituto de Biología y Genética Molecular,
Universidad de Valladolid y Consejo Superior de Investigaciones
Científicas, Departamento de Bioquímica y
Biología Molecular y Fisiología, Facultad de Medicina,
E-47005 Valladolid, Spain; and We have reported that a population of chromaffin cell mitochondria
takes up large amounts of Ca2+ during cell
stimulation. The present study focuses on the pathways for
mitochondrial Ca2+ efflux. Treatment with protonophores
before cell stimulation abolished mitochondrial Ca2+ uptake
and increased the cytosolic [Ca2+]
([Ca2+]c) peak induced by the stimulus.
Instead, when protonophores were added after cell stimulation, they did
not modify [Ca2+]c kinetics and inhibited
Ca2+ release from Ca2+-loaded mitochondria.
This effect was due to inhibition of mitochondrial Na+/Ca2+ exchange, because blocking this system
with CGP37157 produced no further effect. Increasing extramitochondrial
[Ca2+]c triggered fast Ca2+
release from these depolarized Ca2+-loaded mitochondria,
both in intact or permeabilized cells. These effects of protonophores
were mimicked by valinomycin, but not by nigericin. The observed
mitochondrial Ca2+-induced Ca2+ release
response was insensitive to cyclosporin A and CGP37157 but fully
blocked by ruthenium red, suggesting that it may be mediated by
reversal of the Ca2+ uniporter. This novel kind of
mitochondrial Ca2+-induced Ca2+ release might
contribute to Ca2+ clearance from mitochondria that become
depolarized during Ca2+ overload.
Instituto de
Farmacología Teófilo Hernando, Departamento de
Farmacología y Terapéutica, Facultad de Medicina,
Universidad Autónoma de Madrid, E-28029 Madrid, Spain
Corresponding author. E-mail address:
jalvarez{at}ibgm.uva.es.
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