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Biophys J, February 2002, p. 684-692, Vol. 82, No. 2
Department of Physics, National University of Colombia, Medellin Branch, AA3840 Medellin, Colombia
Voltage-dependent anion channels in the outer
mitochondrial membrane are strongly regulated by electrical potential.
In this work, one of the possible mechanisms of the outer membrane
potential generation is proposed. We suggest that the inner membrane
potential may be divided on two resistances in series, the resistance
of the contact sites between the inner and outer membranes and the resistance of the voltage-dependent anion channels localized beyond the
contacts in the outer membrane. The main principle of the proposed
mechanism is illustrated by simplified electric and kinetic models.
Computational behavior of the kinetic model shows a restriction of the
steady-state metabolite flux through the mitochondrial membranes at
relatively high concentration of the external ADP. The flux restriction
was caused by a decrease of the voltage across the contact sites and by
an increase in the outer membrane potential (up to +60 mV) leading to
the closure of the voltage-dependent anion channels localized beyond
the contact sites. This mechanism suggests that the outer membrane
potential may arrest ATP release through the outer membrane beyond the
contact sites, thus tightly coordinating mitochondrial metabolism and
aerobic glycolysis in tumor and normal proliferating cells.
Biophys J, February 2002, p. 684-692, Vol. 82, No. 2
© 2002 by the Biophysical Society 0006-3495/02/02/684/09 $2.00
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