Hypothermia effects on liver and kidney oxidative stress parameters in an experimental model of sepsis in rats

Oxidative stress (OS) seems to be an important mediator of cellular injury, from which sepsis can proceed. Studies have demonstrated the protective effect of controlled hypothermia in sepsis. This study aimed to evaluate its effects on OS parameters in rat hepatic and renal tissue septic after caecal ligation and puncture (CLP). Three groups were appointed (10 rats/group): C (control), SN (sepsis normothermic), and SH (sepsis hypothermic). Ten hours from CLP, the liver and kidneys were harvested and total protein concentration, superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, lipid peroxidation level (malondialdehyde (MDA), carbonylated proteins (2,4-dinitrophenylhydrazine (DNPH), and fatty acid profile were analysed. Sepsis significantly increased SOD and GPx activities in the liver, regardless of the temperature. In renal tissue, GPx activity increased significantly in normothermic conditions and SOD tended to decrease in hypothermic conditions. MDA and DNPH concentrations increase in both tissues after CLP. Hypothermia significantly lowered MDA in the liver but only changed it insignificantly in the kidneys. The DNPH in the liver and kidneys was significantly lower in hypothermic conditions. The unsaturated-to-saturated fatty acids ratio was significantly lower in sepsis, and the fall in temperature raised this ratio. Experimentally induced sepsis in rats enhances OS in the liver and kidneys. The effect of hypothermia on OS indices is dependent on the type of tissue.