@entity5911 - and XXXX -induced calcium efflux from mitochondria occurs by reversal of the uptake pathway.

@entity4323 @entity35 @entity141 @entity34940 @entity37236 @entity17361 @entity5911
1. Addition of @entity5911 or @entity4323 to isolated @entity35 liver mitochondria results in an efflux of @entity141 . Concomitant with this efflux is an immediate oxidation of endogenous @entity34940 , a fall in the mitochondrial membrane potential and an increase in the rate of respiration. The primary effect in this sequence may be either (a) physiologically important stimulation of a @entity141 -efflux carrier, followed by @entity141 re-uptake, a fall in membrane potential and increased respiration, or (b) physiologically unimportant damage to mitochondrial integrity, followed by a fall in membrane potential, increased respiration and @entity141 efflux. 2. @entity37236 and EGTA will restore the increased respiratory rate to one approximating to the control rate of respiration. However, addition of @entity17361 , at a concentration which inhibits the uptake but not the normal efflux of @entity141 , inhibits the rate of @entity141 efflux induced by @entity5911 or @entity4323 . Therefore the observed efflux is occurring by a reversal of the uptake pathway (uniporter) and thus follows the fall in membrane potential. 3. From these results we conclude that the decrease in membrane potential and increase in the rate of respiration seen during @entity5911 - or @entity4323 -induced @entity141 efflux cannot be accounted for by rapid @entity141 cycling, but are due to damage to mitochondrial integrity.
