On the one hand, hyperthermia might increase mitochondrial ROS generation. During normal mitochondrial function, a small percentage of electrons from the electron transport chain reduce oxygen to form superoxide. During mitochondrial dysfunction, this leak of electrons is increased. 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.