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Studies on Mitochondria, III The relationship of structure and function of mitochondria from heart muscle



Studies on Mitochondria, III The relationship of structure and function of mitochondria from heart muscle



Exptl Cell Res 3(1): 42-57



Studies on oxidation by mitochondria established that the maintenance of the cyclophorase complex and the integrity of the structure of mitochondria were interdependent. Obliteration of the internal structure of the mitochondria accompanied cessation of cyclical oxidation, but the relationship appears to be even more precise and positive because several states of the mitochondria affect and appear to govern the rate of oxidation. The shape of mitochondria from heart muscle is correlated with oxidative activity. Osmotic pressure and Mg concn. exert comparable influences on morphology and oxidation. On the other hand, several electrolytes depress oxidation without alteration of mitochondrial structure. The rod forms, which are the usual intracytoplasmic shape in heart muscle, allow only slow oxidation. Although this may appear a paradox, it is not out of place to believe that such a limited rate of oxidation may be more appropriate to the regulated events of the intracellular environment, and that such a dampened effect is also attributable to the high intracellular K levels. The authors' observations indicate that such a salt effect on cellular oxidation is probable. At the opposite extreme the isolated, swollen, crescent-shaped mitochondria have a diminished capacity to metabolize. It is interesting that this is the form which characterizes the peculiar cellular alteration called "cloudy swelling" which is a type of degeneration well known to pathologists. Between these extreme variations there are numerous transitional forms. It is probable that fluctuations in shape and size of the mitochondria, which are amply described in the older literature, may reflect the sequence of metabolic events in the cells and contribute by their metamorphoses to metabolic regulation.

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Accession: 025551079

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DOI: 10.1016/0014-4827(52)90030-x


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