Mitochondrial damage and the proportion of effete mitochondria in cells increase with age. According to the mitochondrial theory of aging, this phenomenon is mostly due to oxidative damage and is a major (and, some argue, the main) determinant of aging. It will be argued briefly that this phenomenon plays a role that is not exclusively crucial in aging. It will also be contended, essentially on theoretical grounds (for lack of sufficient current information), that there is low probability that the accumulation of reduced degradation of affected mitochondria is due to diminished production of hydroxyl radicals, as suggested by Aubrey and de Grey (1997) and expanded by Kowald (in this issue). What seems more likely is that the phagolysosomal disposal system of effete mitochondria is considerably altered in cells of aging organisms. Also, in view of the significant role of damaged mitochondria in the initial steps in apoptosis and the lack of evidence of massive apoptosis of cells in senescent individuals, the damage that exists may be milder than anticipated by the mitochondrial theory of aging. A brief fundamental summary on the biology of mitochondria is included for the sake of better understanding the arguments presented in this article. Also, suggestions are made for experimental testing of the hypotheses presented by Aubrey and de Grey (1997) and Kowald (1999).