IMPAIRED PHOSPHATIDYLCHOLINE BIOSYNTHESIS AND ASCORBIC ACID DEPLETION IN LUNG DURING LIPOPOLYSACCHARIDE-INDUCED ENDOTOXAEMIA IN GUINEA PIGS

作者: Enrique Benito , María A. Bosch

DOI: 10.1023/A:1006883628365

关键词: Shock (circulatory)Phosphatidylcholine BiosynthesisInternal medicineBiologyAntioxidantLipopolysaccharideBiochemistryEndocrinologyLipid peroxidationPhosphatidylcholineLung injuryAscorbic acid

摘要: Injection of guinea pigs with a single dose Escherichia coli lipopolysaccharide (3.2 mg/100 g) induces reversible endotoxic shock that was evaluated by measuring plasma glucose levels and aspartate aminotransferase activity at 24 h after injection. The hypoglycaemia the increase in observed, correlated alterations found during recovery phase shock. When lipid peroxidation some antioxidant systems were measured lungs from treated animals, we only differences ascorbic acid content, decreased 50%. Lipopolysaccharide treatment results depression pulmonary phosphatidylcholine synthesis, correlates surfactant deficiencies associated respiratory illnesses septic Guinea fed on diet low content more sensitive to endotoxin. In these animals no detectable lung, whereas both vi tamin E lung synthesis significantly decreased. Our point out significance protection against oxidative injury endotoxaemia, validate our model for further studies mechanisms this pathological condition. (Mol Cell Biochem 175: 117–123, 1997)

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