Changes in the levels of liver HSP70, plasma nitric oxide, and the antioxidative system in an experimentally induced endotoxemia mouse model and the role of reduced glutathione

Abstract

Endotoxin molecules in lipopolysaccharides are among most important molecules that initiate a cascade of events in sepsis/endotoxemia. Lipopolysaccharide exposure may result in strong immune responses, disrupt the intracellular oxidant/antioxidant balance, and cause excessive reactive oxygen species generation. The purpose of the study was to examine if reduced glutathione (GSH) has a protective role against lipopolysaccharides. The effects of lipopolysaccharide (LPS) or GSH alone or in combination on the levels of the plasma antioxidant system, NO, and liver HSP70 were investigated. A total of 100 Swiss albino mice were divided into 4 groups as Group I (control), Group II (20 μg/kg LPS), Group III (10 mg/kg GSH), and Group IV (20 μg/kg LPS + 10 mg/kg GSH). Blood and liver samples both pre- and post-LPS and/or GSH injections after 1, 3, and 6 h were collected. Total antioxidant capacity was demonstrated with a reduction in response to lipopolysaccharide. Total oxidant capacity was higher after the injection of lipopolysaccharide alone or in combination with GSH. NO levels were elevated in response to lipopolysaccharide. The liver HSP70 level was determined to be higher in the lipopolysaccharide-treated group. These results indicate that exogenously administered GSH may have regulatory effects on liver HSP70 and plasma NO levels, and GSH treatment might have beneficial effects on antioxidant status by inhibiting the increase of oxidant molecules in endotoxemia-induced mice.