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.
