Abstract
It has been generally accepted that NADH (nicotinamide-adenine-dinucleotide) cannot penetrate the inner mitochondrial membrane. Thus NADH generated in the cytoplasm cannot be re-oxidized by the electron transport system unless first transported into the mitochondria by a reduced partner of a suitable cytoplasmic NAD-linked dehydrogenase [10]. The malate-aspartate shuttle appears to be one of the principal ways, in rat liver and heart muscle, by which reducing equivalents are transported. Since the shuttle involves the passage of malate, alpha-ketoglutarate, aspartate and glutamate across the mitochondrial membrane, the possibility exists that the shuttle could be controlled by these intermediates [10]. In other tissues, as well as heart and liver, the malate-aspartate shuttle appears to operate [9].
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Koziol, B.J., Edington, D.W. (1975). The Effects of Prolonged Direct Muscle Stimulation on Biochemicals Associated with the Malate-Aspartate Shuttle in Rat Skeletal Muscle. In: Howald, H., Poortmans, J.R. (eds) Metabolic Adaptation to Prolonged Physical Exercise. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-5523-5_18
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DOI: https://doi.org/10.1007/978-3-0348-5523-5_18
Publisher Name: Birkhäuser, Basel
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