This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Eboli, M. L. Articles by Papa, S. Search for Related Content PubMed PubMed Citation Articles by Eboli, M. L. Articles by Papa, S.

Transport of Anionic Substrates and Glutamate Metabolism in Mitochondria from Ascites Tumor Cells¹

Institute of Biological Chemistry, Faculty of Medicine, Centre for the Study of Mitochondria and Energy Metabolism, C.N.R., University of Bari, Bari [G. P., S. P.], and Institute of General Pathology, Catholic University, Rome Italy [M. L. E.]

A study is presented of -oxoglutarate and glutamate transport and of glutamate oxidation in ascites tumor cell mitochondria.

Kinetics analysis of -oxoglutarate transport in mitochondria from two strains of Ehrlich ascites tumor cells, the hyperdiploid and the hyperdiploid Lettré mutant, shows that the activity of the -oxoglutarate carrier and its affinity for substrates are higher in the mutant than in the wild strain.

Evidence is presented showing the occurrence of carrier-mediated glutamate-OH exchange-diffusion in mitochondria from both strains. The activity of the glutamate carrier is apparently higher in the hyperdiploid Lettré mutant.

Glutamate oxidation occurs mainly through transamination to aspartate in both tumor strains. The rate of deamination in the two strains correlates directly with the level of glutamate dehydrogenase (EC 1.4.1.3.), which is higher in the wild than in the mutant strain. Thus glutamate dehydrogenase per se, and not glutamate penetration, constitutes the control step for glutamate deamination.

Data are presented on the transamination in mitochondria of glutamate with externally added oxaloacetate (arsenite present) that exclude an obligatory transport of oxaloacetate on the -oxoglutarate carrier.

¹ This work was in part supported by a grant of "Consiglio Nazionale delle Ricerche," Rome, Italy, to Professor T. Terranova, Catholic University, Rome, Italy.

² To whom requests for reprints should be addressed, at Istituto di Patologia Generale. Università Cattolica S. Cuore. Via Pineta Sacchetti, 644, 00168 Rome, Italy.

Received 3/ 2/76. Accepted 5/ 7/76.