The primary goal of this research was to determine the effect of the pro-apoptotic protein, Bax, on chronic endogenous oxidative stress. This was accomplished by measuring reactive species (RS) production in cortical neuron cell culture and also by assessing markers of oxidative damage in the aging mouse cortex. It is postulated that the accumulation of RS contributes to the aging process. RS are produced as a natural byproduct of mitochondrial respiration and are normally kept in balance by an extensive antioxidant system. When the RS produced overwhelms this antioxidant system, oxidative stress can occur. The oxidative stress theory of aging proposes damage arising from this process causes aging to occur. The process of aging is compounded by an increasing probability of acquiring age-related disorders, such as Alzheimers and Parkinsons diseases. Neurons are especially vulnerable to RS damage because these cells are post-mitotic, have a high oxygen demand, and relatively low antioxidant capacity. The literature also suggests that apoptosis is involved with the aging process as well. Bax is a pro-apoptotic Bcl-2 family member that is known to enhance RS production in several cell culture models. Cortical neurons are a target for damage in many neurodegenerative diseases as well as in normal aging. It was the goal of this research to understand the effects of Bax on RS production in cortical neurons. A further goal of this project was to understand these effects on oxidative damage in the aging nervous system. Understanding the role of Bax in the aging process may lead to improved therapies for age-related neurodegenerative disease.