A rapidly increasing amount of data supports the view that progressive bioenergetic loss caused by injury of the main energy-producing subcellular organelles, that is, the mitochondria, plays a key role in aging. A link between senescence and energy loss is already implied in Harman’s (1) free radical theory of aging, according to which oxygen-derived free radicals injure the cells, with concomitant impairment of performance at the cellular and physiological levels. Further, Miquel and co-workers (2, 3) have proposed a mitochondrial theory of aging, according to which aging results from oxygen stress damage to the mitochondrial genome, with concomitant bioenergetic decline. More recently, a number of laboratories, including our own (4–6), have provided biochemical data in agreement with the above views. Thus, we have shown that, as the result of age-related oxygen stress, mitochondrial glutathione is oxidized in direct relation to injury of the mitochondrial DNA (5). Further, our studies suggest that an antioxidant product extracted from Ginkgo biloba may counteract in part the damaging effects of free radicals on mitochondrial and cellular aging (7).