title: Mitochondrial consumption of cytosolic ATP: not so fast.
abstract: In various pathologic circumstances depolarized mitochondria are thought to precipitate cell death by avidly consuming cytosolic ATP. However, for as long as the inner mitochondrial membrane remains intact the reversal potentials of the adenine nucleotide translocase (ANT) and that of F(0)-F(1) ATP synthase are strategically positioned so that they oppose import of cytosolic ATP into the matrix of respiration-impaired mitochondria. This arrangement also seems to protect against a hysteretic consumption of cytosolic ATP accumulating in the mitochondrial matrix, in view of the depolarization caused by inhibition of F(0)-F(1) ATP synthase by the endogenous protein IF1, yielding fast ANT reversal rates.
authors.affiliation: Department of Medical Biochemistry, Semmelweis University, Budapest, Hungary. chinopoulos.christos@eok.sote.hu
authors.forename: Christos
authors.initials: C
authors.lastname: Chinopoulos
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000465:Algorithms; D000818:Animals; D003600:Cytosol / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D000226:Mitochondrial ADP, ATP Translocases / Q000378:metabolism*; D051336:Mitochondrial Membranes / Q000378:metabolism; D008954:Models, Biological; D006180:Proton-Translocating ATPases / Q000378:metabolism*
chemical_list: D000255:Adenosine Triphosphate; D000226:Mitochondrial ADP, ATP Translocases; D006180:Proton-Translocating ATPases