Evidence for the presence of a reversible Ca2+-dependent pore activated by oxidative stress in heart mitochondria.
Rat heart mitochondria became permeabilized to sucrose when incubated with 100 nmol of Ca2+/mg of protein in the presence of Pi. Ca2+ chelation with EGTA restored impermeability to sucrose, which became entrapped in the matrix space. t-Butylhydroperoxide markedly promoted permeabilization in the presence of Ca2+ but not in its absence, and Ca2+-plus-t-butylhydroperoxide-induced permeabilization was reversed by EGTA. The data suggest that Ca2+ and oxidative stress synergistically promote the reversible opening of an inner membrane pore.
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D004533:Egtazic Acid / Q000494:pharmacology; D007202:Indicators and Reagents; D007425:Intracellular Membranes / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D009861:Onium Compounds; D009943:Organophosphorus Compounds; D010100:Oxygen / Q000378:metabolism; D010539:Permeability; D010545:Peroxides / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D020122:tert-Butylhydroperoxide
D007202:Indicators and Reagents; D009861:Onium Compounds; D009943:Organophosphorus Compounds; D010545:Peroxides; D004533:Egtazic Acid; D020122:tert-Butylhydroperoxide; D010100:Oxygen; D002118:Calcium; C013289:tetraphenylphosphonium