Release of mitochondrial matrix proteins through a Ca2+-requiring, cyclosporin-sensitive pathway.
Induction of the inner membrane permeability transition, normally associated with the release of small molecules and ions from the mitochondrial matrix, also causes the release of matrix proteins. The release is linear with time and slow when compared to the time course of mitochondrial swelling. Transient induction of the high permeability state is reflected in transient release of proteins. Cyclosporin A (0.5 nmol/mg protein) or chelation of free Ca2+, which reverses the permeability transition, also block the subsequent release of protein even when added after extended preincubation. Possible mechanisms of protein release are discussed.
Igbavboa
U
U
Hormel Institute, University of Minnesota, Austin 55912.
Zwizinski
C W
CW
Pfeiffer
D R
DR
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000502:physiology*; D003524:Cyclosporins / Q000494:pharmacology*; D004533:Egtazic Acid / Q000494:pharmacology; D008291:Malate Dehydrogenase / Q000378:metabolism; D008930:Mitochondria, Liver / Q000378:metabolism*; D008970:Molecular Weight; D010539:Permeability; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D003524:Cyclosporins; D011506:Proteins; D004533:Egtazic Acid; D008291:Malate Dehydrogenase; D002118:Calcium