Age-induced hair graying (canities), or the age-induced loss of melanin synthesis and deposition within the hair shafts, is a noticeable and undesired sign of the aging process. Numerous mechanisms contribute to age-induced hair graying, affecting both follicular and stem cell melanocytes and acting at different follicular locations. Many of these processes are induced, directly or indirectly, by oxidative insults and damage. Melanin-producing bulbar melanocytes express high levels of BCL-2 to survive reactive oxygen species (ROS) attacks, which are induced by the melanogenic process itself and by ultraviolet A (UVA) irradiation. With aging, the expression of BCL-2, and possibly of TRP-2, is reduced, and the endogenous, enzymatic antioxidant defense system declines, resulting in greater oxidative stress. In particular, catalase expression and activity are markedly reduced with aging, leading to millimolar accumulation of hydrogen peroxide within the hair follicle and contributing to bulbar melanocyte failure and death. Additionally, exposure of melanocyte stem cells to cumulative oxidative damage, combined with reduced BCL-2 protective levels, results in apoptosis and therefore decreases the number of melanocytes that could repopulate the newly formed anagen follicles. Altogether, oxidative stress may contribute to age-induced hair graying via multiple pathways. Better understanding of the different processes, sources, and types of oxidative stress within the follicular environment, and the different susceptibilities of melanocytes to oxidative stress at the different follicular locations, might yield clues to possible interventions for prevention or reversal of hair graying.