Bcl-2 is a key regulator of the intrinsic pathway by interfering with cytochrome C release through its interaction with Bax [51]. Other studies have shown that mitochondrial ROS easily oxidized cardiolipin, and oxidized cardiolipin appears to be essential for mitochondrial membrane permeabilization and release of pro-apoptotic factors into the cytosol [52]. Conversely, prevention of cardiolipin peroxidation leads to inhibition of apoptosis [53]. These findings suggest that cardiolipin might be a crucial molecule that regulates the initiation of apoptosis. Our data demonstrate that hyperthermia increased cardiolipin peroxidation and that mitochondrial ROS plays an important role in hyperthermia-induced cardiolipin peroxidation. Future studies will investigate whether cardiolipin peroxidation plays an important role in initiating hyperthermia-induced platelet apoptosis.