Oxidation and Phosphorylation in Liver Mitochondria Lacking "Polymerized" Ribonucleic Acid

The administration of cortisone to rats and rabbits has been found to cause profound changes in the hepatic parenchyma; i.e . . . . increase in cell size, accumulation of glycogen, and greatly decreased cytophsmic basophilia which has been found not to be decreased further by treatment with ribonudease (1-4). Microscopic examination has also indicated a decrease in numbers of mitochondria and alterations in their morphology (5). Mitochondria isolated by differential centrifugation of homogenates of such livers in either saline (4) or 0.25 M sucrose (6) have been found to be completely devoid of ethanolprecipitable riboundeic acid (presumably highly polymerized forms of RNA). In addition the microsomes from such livers were found to contain little or no ethanolprecipitable RNA. These effects of cortisone are reversible; within 8 days after cessation of treatment the liver picture is essentially normal (4). The apparent lack of polymerized RNA in such mitochondria is a point of special interest. Although it has often been suggested that the KNA found in isolated mitochondria derives from contaminating microsomes (c/. 7, 8), even