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With the recognition that the imbalance between oxidant and antioxidant compounds is an important causative agent of aging and of various chronic diseases (
1
), there has been growing interest in elucidating the pathways involved in oxidative-stress initiation. As oxidative stress is an inescapable repercussion of aerobic life, all organisms that use oxygen protect themselves against free radicals (
1
). Although cells are endowed with impressive equipment of antioxidant defenses (
2
), they are not completely efficient to resist an increased free-radical formation.