Conformational basis of energy transduction in mitochondria
The conformational mechanism of energy transduction which we proposed in 1967 was based on an intuitive evaluation of the significance of large amplitude configurational changes which parallel energized processes in mitochondria [l-3] . By now a considerable body of information has been accumulated about the details of the configurational transitions in the mitochondrion [4-61. Moreover, the theory of structured systems with the capability for conservation of energy by a conformational mechanism is now being developed systematically [7]. This interplay of experiment and theory has made it possible to formulate the conformational hypothesis more explicitly and precisely. The tripartite repeating unit of the cristal membrane is the molecular unit of mitochondrial energy transduction. While in theory each repeating unit is a complete operational unit, in practice we are dealing with two dimensional arrays of repeating units within a membrane continuum and with the cooperative effects intrinsic to such arrays. Each repeating unit contains three basic systems which collectively effectuate the conformational transduction of energy. These systems are (a) the primary energizing system (one of the complexes of the electron transfer chain), (b) the conformational frame system, and (c) the discharge-directing system (the ATPase complex is one such system). The electron transfer process within each complex of the chain leads to a conformational transition [8-lo]. But since the electron transfer system is enclosed within a rigid frame (the conformational frame system [ 7]), the conformational expansion of
Biochemical lesions of respiratory enzymes and configurational changes of mitochondria in vivo
SummaryCorrelative biochemical and electron microscopic alterations were observed in chick embryo myoblasts in vitro after treatment with fluoroacetate. Fluoroacetate poisoning caused an increase of citrate and a decrease of ATP in the cultures. Cell respiration was only slightly impaired by fluoroacetate in the first 10 min but was inhibited to 30% one hour after exposure to the poison. Fluoroacetate did not affect oxidative phosphorylation. The evidence suggests that fluoroacetate was transformed in myoblasts into fluorocitrate which inhibited the mitochondrial-bound aconitate hydratase as in adult tissues. Ultrastructural changes in the majority of the fluoroacetate-treated cells were observed. Very few myoblasts appeared unaffected by the poison. Mitochondria were specifically altered. The early changes occurred in the mitochondrial matrix where the inhibited enzyme is known to be located and were followed by modifications in the configuration and structure of cristae. Exogenous fluorocitrate caused ultrastructural changes in the mitochondria similar to that provoked by fluoroacetate. The localization of the early change in the mitochondrial matrix and the evaluation of the structural modifications suggest a correlation between the biochemical lesion, i.e. the inhibition of aconitate hydratase, and the change revealed in the mitochondrial structure containing the inhibited enzyme.
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