Fig. 4. Altered mitochondrial bioenergetics seems to be central to a variety of physiologic and pathophysiological states that share oxidative stress as a common characteristic. Despite the protective effects ( dashed lines ) of DNA repair mechanisms, endogenous antioxidants, and antiapoptotic substances such as heat shock proteins (HSPs), some of which may be further stimulated by ischemic or anesthetic preconditioning (IPC/APC), oxidative stress eventually disrupts the mitochondrion and triggers rapid mitochondrial and cellular self-destruction (mitoptosis and apoptosis).