In vitro transport of F1-ATPase beta-subunit into mitochondria of Zajdela hepatoma and rat liver.

Transport of precursor of F1-ATPase beta-subunit into isolated mitochondria of Zajdela hepatoma and rat liver was examined. The hepatoma mitochondria were more active in the process than the liver organelles indicating that the relative F1-ATPase deficiency in the tumor mitochondria does not result from an impaired transport of F1-ATPase subunits into the tumor organelles. Similar results were obtained using digitonin-treated rat hepatocytes and Zajdela hepatoma cells instead of isolated mitochondria. The suitability of the digitonin-treated cells in the study of protein transport into mitochondria in vitro is demonstrated and the advantages of this system over isolated mitochondria are discussed.