Glutamine transport by mitochondria isolated from normal and acidotic rats.
The transport of L-glutamine by isolated rat renal mitochondria was studied by means of a rapid-filtration (Millipore Filter Corp.) technique. The movement of glutamine from the incubation medium into the inner mitochondrial compartment (matrix) was inhibited by structural analogues (6-diazo-5-oxo-L-norleucine and glutamic acid), sulghydryl-binding agents (p-chloromercuri-benzoate and mersalyl), and inhibitors of mitochondrial oxidative metabolism (azide, antimycin A, and uncouplers of oxidative phosphorylation). These results suggest that glutamine is transported across the inner membrane of renal mitochondria by a carrier-mediated system that is linked to the processes of oxidative metabolism. The transport of glutamine by isolated renal mitochondria was increased two- to threefold by chronic (5-7 days) metabolic acidosis. However, short-term metabolic acidosis did not increase the glutamine transport capacity of isolated mitochondria. A hypothesis is presented for the regulation of mitochondrial glutamine transport, in vivo, during short-term and chronic acidosis.
D000138:Acidosis / Q000378:metabolism*; D000222:Adaptation, Physiological; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D003864:Depression, Chemical; D003980:Diazooxonorleucine / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005973:Glutamine / Q000378:metabolism*; D007668:Kidney / Q000648:ultrastructure; D007700:Kinetics; D008297:Male; D008566:Membranes / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism* / Q000648:ultrastructure; D051381:Rats
D000596:Amino Acids; D004791:Enzyme Inhibitors; D003980:Diazooxonorleucine; D005973:Glutamine