Energy-driven aspartate efflux from heart and liver mitochondria.

The et&x of aspartate from rat heart and liver mitochondria is facilitated by energy derived from the electron transport chain or from adenosine triphosphate. The metabolic significance of this finding resides in the fact that aspartate efflux from mitochondria is required for operation of the malate-aspartate cycle, which is a major pathway for the energy-requiring transport of reducing equivalents from the cytosol to the mitochondrial matrix. The experiments described represent an attempt to elucidate the mechanism by which provision of a source of metabolic energy interacts with the transport system. In order to study efflux rates, aspartate was generated inside the mitochondria from glutamate and malate. Transport constants were estimated by measuring both intraand extramitochondrial aspartate. The ionophore, valinomycin, inhibited transport in the presence of high concentrations of K+ but stimulated transport in the absence of K+ while the ionophore nigericin had no effect. Extramitochondrial phosphate stimulated transport of aspartate in the absence of measurable phosphate movement across the membrane. The data indicate that aspartate transport is facilitated by the presence of an electrical potential gradient across the mitochondrial membrane.