Studies on the efflux of metalloporphyrin from isolated rat liver mitochondria. Effect of respiratory substrates and metabolic inhibitors.
Intramitochondrially synthesized Co-deuteroporphyrin is released to the incubation medium at a rate inversely correlated to the energy state of the mitochondria; i.e. the rate of efflux increases when substrate is depleted, respiration inhibited or the mitochondria are uncoupled. The efflux of Co-deuteroporphyrin from mitochondria remains low as long as the residual membrane potential is above one-third that of maximally energized mitochondria. Globin enhances the efflux of Co-deuteroporphyrin not only from mitochondria depleted of substrates [Husby & Romslo (1980) Biochem. J. 188, 459-465], but also from maximally energized mitochondria. The results provide further evidence for a co-operative mechanism between the mitochondria and their surroundings for the mobilization of metalloporphyrin from mitochondria.
D000818:Animals; D000963:Antimetabolites / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone / Q000494:pharmacology; D003035:Cobalt / Q000378:metabolism; D003905:Deuteroporphyrins / Q000378:metabolism; D066298:In Vitro Techniques; D008665:Metalloporphyrins / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D013053:Spectrophotometry; D013997:Time Factors
D000963:Antimetabolites; D003905:Deuteroporphyrins; D008665:Metalloporphyrins; D003035:Cobalt; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone