Isolated mitochondria are capable of undergoing dramatic reversible ultrastructural transformations between a condensed and an orthodox conformation. These two conformations are the extremes in ultrastructural organization between which structually and functionally intact mitochondria transform during reversible respiratory cycles. It has been found that electron transport is required for the condensed-to-orthodox ultrastructural transformation which occurs in mitochondria under State IV conditions, i.e., under conditions in which exogenous substrate is present and ADP is deficient. Inhibition of State IV electron transport at the cyanide-, antimycin A-, or Amytal-sensitive sites in the respiratory chain results in inhibition of this transformation. Resumption of electron transport in initially inhibited mitochondrial systems, initiated by channeling electrons through pathways which bypass the inhibited sites, results in resumption of the ultrastructural transformation. The condensed-to-orthodox transformation is DNP insensitive and, therefore, does not require participation of the coupling enzymes of the energy-transfer pathway. It is concluded that this ultrastructural transformation is manifest by the conversion of the chemical energy of electron transport directly into mechanical work. The reversed ultrastructural transformation, i.e., orthodox-to-condensed, which occurs during ADP-activated State III electron transport, is inhibited by DNP and parallels suppression of acceptor control and oxidative phosphorylation. Mechanochemical ultrastructural transformation as a basis for energy transfer in mitochondria is considered with respect to the results presented.
ULTRASTRUCTURAL BASES FOR METABOLICALLY LINKED MECHANICAL ACTIVITY IN MITOCHONDRIA : II. Electron Transport-Linked Ultrastructural Transformations in Mitochondria
Charles R. Hackenbrock; ULTRASTRUCTURAL BASES FOR METABOLICALLY LINKED MECHANICAL ACTIVITY IN MITOCHONDRIA : II. Electron Transport-Linked Ultrastructural Transformations in Mitochondria . J Cell Biol 1 May 1968; 37 (2): 345–369. doi: https://doi.org/10.1083/jcb.37.2.345
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