Abstract
The effects of actinomycin D on newborn rat liver were studied by using biochemical assays, electron microscopy, and quantitative morphometry. Actinomycin prevented the normal postnatal rise in acid a 1,4 glucosidase (maltase) activity and the breakdown of lysosomal glycogen. The results suggest that the postnatal increase in acid glucosidase activity is protein synthesis dependent. This enzyme is critical for the catabolism of the lysosomal glycogen in newborn rat hepatocytes.