Tissier et al. have previously reported that mild hypothermia preserves mitochondrial function and reduces mitochondrial ROS generation [44]. On the contrary, dysfunction in mitochondrial respiration might increase the formation of ROS in mitochondria [45,46], Swerdlow et al. also reported that enhanced production of mitochondrial ROS was linked to mitochondrial dysfunction [47]. It has also been reported that hyperthermia could induce mitochondrial dysfunction [48] and thus augment mitochondrial ROS production. On the other hand, hyperthermia might provoke decreased antioxidant capacity in mitochondria. Our studies found that hyperthermia caused a decrease of MnSOD activity in platelets. This observation might partly explain the accumulation of mitochondrial ROS in hyperthermia-treated platelets.