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.

中暑和严重发烧会导致贫血，但其潜在机制仍不清楚。在这里，我们报告了使用氧化铈纳米粒子保护红细胞免受短期高温（42°C，10 分钟）造成的损害。与正常生理环境下（37℃，10分钟）相比，热疗红细胞呈现出更高密度、更小尺寸和更低的zeta电位的引渡衰老。此外，与正常条件相比，暴露于高温的细胞表现出显着更高的活性氧 (ROS) 产生。重要的是，使用二氧化铈纳米粒子 (CNPs) 的预处理通过降低 ROS 水平来改善被热疗损伤的红细胞的衰老和凋亡。概括地说，短期热疗引起红细胞中活性氧显着增加，并导致衰老和凋亡。这些可能是暴露于中暑或严重发烧的红细胞病理变化的可能机制。总体而言，这些发现表明 CNP 强烈抑制 ROS 的产生，并有效地改善了热疗引起的红细胞损伤。