Mechanisms of pathogenesis in Listeria monocytogenes infection. VI. Oxidative phosphorylation in mouse liver mitochondria during experimental listeriosis.

Previous reports have demonstrated early changes in hepatic carbohydrate and energy metabolism in mice infected with Listeria monocytogenes. This study was undertaken to further elucidate mechanisms of damage involved in these changes. Female CD-1 mice were injected intraperitoneally with 10(6)L. monocytogenes A4413. At 0, 10, and 20 hr after infection, groups of mice were sacrificed and the livers were removed and pooled. Oxidative phosphorylation was assayed immediately upon isolation of mitochondria from pooled liver homogenates. Appropriate metabolic inhibitors were employed to examine each of the three phosphorylation sites in mitochondrial electron transport. When pyruvate-malate (equimolar concentrations) and alpha-ketoglutarate were used as substrates, decreases in both phosphorylation and oxidation were noted as early as 10 hr after infection. With beta-hydroxybutyrate and citrate as substrates, alterations were not noted until 20 hr after infection, whereas no changes were seen when glutamate, succinate, or ascorbate were employed. These results suggest possible derangement of the first site in oxidative phosphorylation as well as lowered activity of nicotinamide adenine dinucleotide-linked dehydrogenases during experimental listeriosis in mice.