Heat stroke and severe fever cause anemia, although the underlying mechanism remains unclear. Here, we report the use of Cerium oxide nanoparticles in protection of red blood cells against damage caused by exposure to short-term hyperthermia (42°C, 10 min). Red blood cells exposed to hyperthermia exhibited extradition senescence with higher density, smaller size and lower zeta potential relative to those under normal physiological environment (37°C, 10 min). Furthermore, hyperthermia-exposed cells exhibited significantly higher reactive oxygen species (ROS) production compared to the normal conditions. Importantly, the preconditional treatment, using Ceria nanoparticles (CNPs), ameliorated senescence and apoptosis in red blood cells damaged by hyperthermia by reducing ROS levels. Summarily, short-term hyperthermia caused a significant increase in ROS in red blood cells, and resulted in senescence and apoptosis. These may be possible mechanisms of pathological changes in red blood cells exposed to heat stroke or severe fever. Overall, these findings indicate that CNPs strongly inhibit ROS production, and effectively ameliorates hyperthermia-induced damages in red blood cells.
Expression of human thrombomodulin on porcine endothelial cells can reduce platelet aggregation but did not reduce activation of complement or endothelium – an experimental study
