Increased hepatic phosphatidylcholine hydroperoxide and deteriorated hepatic energy metabolism in rats with endotoxemia

Liver dysfunction has been observed during severe nonhepatic infection with gram-negative bacteria; however, the pathogenesis of this clinical manifestation remains obscure. This study was designed to see the effect of endotoxemia on the oxidation product of one of the major classes of lipids associated with hepatocellular membrane, i.e. hepatic phosphatidylcholine hydroperoxide (PCOOH). The relations between PCOOH, hepatic energy charge and hepatic blood flow were also investigated. Cecal ligation and puncture (CLP) for the induction of endotoxemia were performed in rats. Compared to levels before CLP the serum endotoxin and hepatic PCOOH increased significantly (p < 0.05, p < 0.001 and p < 0.01, P < 0.001, respectively), corresponding to a significant fall of hepatic energy charge (p< 0.05, p< 0.005) 12 and 24 h after CLP. After 12 h of CLP α-tocopherol increased significantly (p < 0.05) but declined at 24 h. Hepatic blood flow remained unchanged throughout the experiment. Elevated lipid peroxidation, likely resulting from endotoxemia rather than hepatic hypoperfusion, may be attributable to impaired hepatic energy metabolism.