Free radical theory of aging pointed out at major rogues responsible for human aging - reactive oxygen and nitrogen species. This conclusion was supported by many studies, but one of the most important question is still remaining unanswered: How aging processes start in healthy humans who do not suffer from any pathological disorders and all the stimuli of pathological disorders are excluded? Of course it is a purely hypothetical question, but if we can select "the physiological component" of aging initiation, it could be of importance for the understanding of a mechanism of aging. Contrary to former suggestions, we are now aware that reactive free radicals are formed in living organisms not only due to interfering of external factors or as a consequence of pathological disorders but as the potent participants of enzymatic reactions and signaling processes. However it is wrong to consider free radicals as the fully tame species; being diffusion-free molecules they are able to escape the most strictly regulated enzymatic processes and start free radical-mediated damage, an origin of aging. In the present work we consider the potential mechanism of aging processes initiated by superoxide formed as a side product of the enzymatic reactions catalyzed by lipoxygenase and cyclooxygenase under physiological conditions. We suggest that superoxide escaped from these enzymatic cycles initiates nonenzymatic lipid peroxidation leading to the formation of prostanoids (isoprostanes), which toxic action is already well documented. Another dangerous way of starting aging processes is the already known superoxide-stimulated mitochondrial aging. This free radical point of view suggests at importance of applying the nontoxic antioxidant supplements capable of reacting with superoxide without producing other much more reactive free radicals. Correspondingly we consider the potential efficacy of major antioxidants (vitamins E and C, flavonoids, SOD mimics, etc.) for fighting against "physiological aging."