The Effect of Streptococcus pneumoniae infection on Peroxisomal Fatty Acid Oxidation

Abstract

Previous data on rats inoculated with S. pneumoniae have shown decreased hepatic ketogenesis as measured by the production of ketone bodies from livers perfused with oleic acid. However, no differences were observed in the ability of isolated mitochondria to oxidize long- chain fatty acids. Since peroxisomes are also involved in the oxidation of long-chain fatty acids, the possibility of their involvement in the intrahepatic control of ketogenesis during S. pneumoniae infection was examined. Liver homogenates from 46-h fasted- control and fasted-infected rats were fractionated by isopycnic sucrose density gradient centrifugation. Fractions were characterized by the following marker enzymes: 5'-nucleotidase (plasma membranes); glutamate dehydrogenases (mitochondria); N-acetyl--glucosaminidase (lysosomes); NADPH cytochrome c reductase (endoplasmic reticulum); and catalase (peroxisomes). KCN-insensitive oxidation of palmitoyl-CoA and fatty acid ligase were measured. A 50% decrease in catalase activity was found in the peroxisomal-rich fractions of infected rats compared to controls but no change was observed in the palmitoyl-CoA oxidizing system or fatty acid ligase. Hence, neither the palmitoyl-CoA oxidizing system nor the fatty acid ligase of the peroxisomal-rich fraction appear to be responsible for the reduced rate of ketone body formation associated with infectious illness.