RESUMEN
The aim of this study was to investigate the contribution of acute alcohol in sepsis-related liver damages using a Cecal Ligation and Puncture (CLP) model. Rats were divided into 7 groups (5 rats/group): control (saline-injected), sham-operated, CLP, ethanol (1.0 and 2.0 g/kg b.w) and CLP+ethanol. The CLP+ethanol group received a single dose of ethanol following sepsis induction. Sepsis induction caused early changes in lipid peroxidation products in liver, whereas ethanol alone (2.0 g/kg b.w) resulted in a significant increase (~21%) in lipid peroxidation, which was further increased (~57%) in CLP rats treated with alcohol. CLP operation and alcohol treatment exhibited additive effects on plasma catalase, liver glutathione and glutathione S-transferase (GST), which were primarily suppressed due to ethanol. Hepatic cytochrome P4501A1, which was elevated in CLP rats, was reversed in the CLP+ethanol group. Plasma tumor necrosis factor-α was markedly elevated (~85%) in septic rats, but was unaffected in septic rats having received ethanol. Histopathological observations revealed that inflammatory reactions in liver in response to CLP operation are not intensified by ethanol administration. On the basis of biochemical and histopathological results, it can be concluded that acute ethanol treatment is responsible for early changes in oxidative stress, which may lead to polymicrobial sepsis-related organ damage.