ABSTRACT

The life cycle of virtually all multicellular animals follows the common pattern where the initial stages, dominated by growth and maturation, culminate in the reproductive phase, which is followed by an era of gradual, progressive, and irreversible decline in the efficiency of homeostatic mechanisms, eventually re­ sulting in death. The purpose of current gerontological research is not only to understand the nature of the deleterious senescent changes but, more importantly, to determine what causes or initiates the alterations. An increasing body of evi­ dence suggests that mitochondria play a dual role in the aging process stemming from being the generators of both reactive oxygen species (ROS) and ATP. It is hypothesized that mitochondria, the main intracellular sites of oxygen consump­ tion and generation of ROS, are also the main targets of ROS-inflicted damage, resulting in a progressively decreasing ability to synthesize ATP, which conse­ quentially lowers the homeostatic ability to adapt to the destabilizing effects of external and/or internal stresses. Several lines of evidence collectively provide credence to this hypothesis. This chapter focuses on the effect of aging on mito­ chondrial ROS generation and protein oxidative damage, and the roles of mito­ chondrial coenzyme Q and vitamin E in protection against ROS.