Permeability Pathways of Ca2+ Efflux from Mitochondria: H+ Specificity and Reversibility of the Permeability Defect
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During the 1970’s it was established that the inner membrane of isolated mitochondria from adrenal cortex, heart, and liver can display an unusually high permeability to small molecules and ions following the imposition of certain metabolic conditions (1–10). Generally, what is required to produce the permeable inner membrane state is energy-dependent Ca2+ accumulation preceding or following the administration of another agent which is often referred to as a “Ca2+ -releasing agent” (11–14). Substances possessing “Ca2+-releasing agent” activity normally lack detergent properties and are diverse with respect to their chemical properties and biological activities. The “Ca2+-releasing agents” investigated by our group include N-ethylmaleimide (5, 6, 11, 13, 15), t-butylhydroperoxide (14–16), oxalacetate, (11), inorganic phosphate (11, 13), rhein (16), and hypolipidemic drugs such as WY-14643 and dofibric acid (17).
KeywordsLiver Mitochondrion Malignant Hyperthermia Matrix Space Permeability Defect Succinate Oxidation
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