Abstract
The present studies investigate the basis for the marked increase in mitochondrial size and approximately reciprocal decrease in mitochondrial number which have been observed in the livers of rats treated with cortisone acetate. Comparisons of the content and specific activity of mitochondrial DNA in the livers of control and cortisone-treated animals prelabeled with radioactive thymidine support the possibility that these changes in mitochondrial size and number are the result of a process of mitochondrial fusion. A consideration of various conditions now known to result in the formation of large mitochondria in other systems suggests that interference with mitochondrial respiration may provide a stimulus for such a process. The biochemical approach described in the present study may prove useful in investigating the origin of large mitochondria in other systems as well.