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Subcellular Distribution of Branched-Chain Aminotransferase Activity in Rat Tissues^1,2,

Department of Physiology, The Milton S. Hershey Medical Center of the Pennsylvania State University, Hershey, PA 17033

The activity of branched-chain aminotransferase in mitochondria isolated from rat tissues was examined, and the mitochondrial contribution to total tissue branched-chain aminotransferase activity was calculated using the mitochondrial marker enzyme citrate synthase. Mitochondrial aminotransferase activity was highest in heart followed by skeletal muscle, kidney and brain. In heart muscle all of the aminotransferase activity was accounted for by the mitochondrial fraction. Activity was found to be mitochondrial in skeletal muscle with high red fiber content and also in kidney cortex. Activity was predominantly cytosolic in brain and muscles with high white fiber composition. Thus, the distribution of branched-chain aminotransferase activity in skeletal muscle was dependent on fiber type. No branched-chain aminotransferase activity was detected in liver mitochondria, and in liver tissue activity was too low to be relevant at physiological concentrations of branched-chain amino acids. Within a tissue, regardless of the subcellular distribution of aminotransferase activity, the relative rates of transamination with subsaturating or "saturating" concentrations of KIV or isoleucine were similar. Finally, amino acid preference was also similar within a tissue, but not necessarily between or among different tissues.

KEY WORDS: • branched-chain aminotransferase • branched-chain amino acids • mitochondrial transamination

¹ Supported by Grant No. DK34738 from the National Institutes of Health, United States Public Health Service, Bethesda, MD.

² Presented in part at the International Conference on Integration of Mitochondrial Function, Chapel Hill, NC, in June, 1987.

³ Present address: Department of Biochemistry, Wake Forest University, Bowman Gray School of Medicine, Winston-Salem, NC 27103.

Manuscript received 7 June 1988. Revision accepted 15 August 1988.

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