Sepsis Induces Diaphragm Electron Transport Chain Dysfunction and Protein Depletion

Sepsis significantly alters skeletal muscle mitochondrial function, but the mechanisms responsible for this abnormality are unknown. We postulated that endotoxin elicits specific changes in electron transport chain proteins that produce derangements in mitochondrial function. To examine this issue,...

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Bibliographic Details
Published in:American journal of respiratory and critical care medicine 2005-10, Vol.172 (7), p.861-868
Main Authors: Callahan, Leigh A, Supinski, Gerald S
Format: Article
Language:English
Subjects:
Abdomen
Adenosine triphosphate
Adenosine Triphosphate - biosynthesis
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Biological and medical sciences
Diaphragm - metabolism
Electron Transport Chain Complex Proteins - physiology
Electrophoresis, Polyacrylamide Gel
Emergency and intensive care: infection, septic shock
Emergency and intensive care: techniques, logistics
Hypotheses
Intensive care medicine
Intensive care unit. Emergency transport systems. Emergency, hospital ward
Male
Medical sciences
Mitochondria
Mitochondria, Muscle - physiology
Mitochondrial Diseases - physiopathology
Multienzyme Complexes - analysis
Musculoskeletal system
NADH, NADPH Oxidoreductases - analysis
Oxygen Consumption
Proteins
Protons
Rats
Rats, Inbred Strains
Respiration
Sepsis
Sepsis - physiopathology
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Summary:Sepsis significantly alters skeletal muscle mitochondrial function, but the mechanisms responsible for this abnormality are unknown. We postulated that endotoxin elicits specific changes in electron transport chain proteins that produce derangements in mitochondrial function. To examine this issue, we compared the effects of endotoxin-induced sepsis on mitochondrial ATP (adenosine triphosphate) formation and electron transport chain protein composition. Diaphragm mitochondrial oxygen consumption and mitochondrial nicotinamide adenine dinucleotide, reduced form, oxidase assays were measured in control rats (n=13) and rats given endotoxin (8 mg/kg/d) for 12 (n=14), 24 (n=14), 36 (n=14), and 48 h (n=13). Electron transport chain subunits from Complexes I, III, IV, and V were isolated using Blue Native polyacrylamide gel electrophoresis techniques. Endotoxin administration: 1) elicited large reductions in mitochondrial oxygen consumption (e.g., 201+/-3.9 SE natoms O/min/mg for controls and 101+/-4.5 SE natoms O/minutes/mg after 48 h endotoxin, p
ISSN:1073-449X
1535-4970
DOI:10.1164/rccm.200410-1344OC