Action of bacterial lipopolysaccharide on the respiration of mouse liver mitochondria.
Escherichia coli O127:B8 lipopolysaccharide (LPS) inhibited oxygen consumption by isolated mouse liver mitochondria at 10 micrograms of LPS per mg of protein when glutamate + malate was the substrate and adenosine 5'-diphosphate had been added (state 3 respiration), but had little effect when adenosine 5'-diphosphate was not added (state 4 respiration). LPS stimulated state 4 respiration at 10 micrograms/mg of mitochondrial protein when succinate was the substrate but had little effect on state 3 respiration. Lipid A from Shigella sonnei at 2 micrograms/mg of mitochondrial protein also stimulated state 4 respiration but did not affect state 3 respiration with succinate as the substrate. Lipid A, unlike LPS, caused a decrease in the adenosine 5'-diphosphate/O ratio. LPS at 100 micrograms/mg of mitochondrial protein impaired the reduction of cytochromes aa3, c, and b when succinate was the substrate but not when reduced nicotinamide dinucleotide, dithionite, or glutamate was the substrate.
D000818:Animals; D004579:Electron Transport / Q000187:drug effects; D004926:Escherichia coli; D008070:Lipopolysaccharides / Q000494:pharmacology*; D051379:Mice; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects*
D008070:Lipopolysaccharides