Arginine transport into fat body mitochondria of the blowfly, Aldrichina grahami, during larval growth

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Osmotic swelling tests show that neither arginine + nor K + passes into the matrix of nonrespiring fat body mitochondria isolated from 4 day old larvae and that arginine + or K + passes through the membrane of nonrespiring fat body mitochondria of 6 day old larvae. This means that the selective transport system of small ions in the fat body mitochondrial membrane is lost after the larva stops eating. Thus, the arginine transport system in the fat body mitochondria of 4 day old larvae was examined. When succinate was added to arginine solutions in which mitochondria were suspended, arginine + readily entered the mitochondria if a permeant proton-yielding anion such as phosphate or acetate was present. However, permeant anions such as nitrate or chloride, which pass through the membrane without carrying protons, do not support arginine + entry. Antimycin, FCCP and DNP completely inhibited the succinate-induced swelling in the solutions containing arginine phosphate and acetate. The succinate-induced swelling in the solutions containing arginine phosphate and acetate was not affected by NEM and oligomycin. The driving force for entry of arginine + is concluded to be a negative inside-transmembrane potential produced when proton-conducting anions enter mitochondria to relieve the alkaline-inside pH gradient generated by electron transport. It is postulated that arginine + is transported by a specific electrogenic uniport carrier.