Oxidative stress plays a central role in the physiological aging process. Caloric restriction mitigates oxidative stress by decreasing the rate of generation of endogenous damage, mechanism that can contribute to the slowing of aging rate induced by this intervention. Various facts recently link methionine to aging: i) it is known that methionine restriction (MetR) without energy restriction increases maximum life span in rats and mice; ii) protein methionine content is inversely related to maximum life span in mammals which makes sense since methionine is among the protein amino acids most susceptible to oxidation by free radicals; iii) methionine dietary supplementation damages many vital organs (like cardiovascular system, liver and nervous system) and increases oxidative stress. Toxic effects of dietary methionine have been related to its conversion to and increase in homocysteine levels. Homocysteine levels also increase with age in humans and represent a risk factor for aging and free radical-associated degenerative diseases; iv) knocking out methionine sulfoxide reductase A -an enzyme which reduces methionine sulfoxide back to methionine through a thioredoxin-dependent reaction- lowers maximum longevity and increases protein carbonyls in mice, whereas overexpression of this enzyme in Drosophila increases its life span and delays aging; v) overexpression of thioredoxin increases longevity in mice; and vi) long-lived mutant Ames dwarf mice seem to have altered methionine metabolism. Available evidences clearly demonstrate that MetR modulates the decrease in endogenous oxidative damage. Thus, it is hypothesized that methionine plays a central role in the aging process.