ABSTRACT
Oxygen-derived free radicals are generated during metabolism and energy pro-
duction in the body and are involved in countless processes such as the regulation
of signal transduction and gene expression, activation of receptors and nuclear
transcription factors, oxidative damage to cell components, the antimicrobial and
cytotoxic action inherent in immune system cells, as well as in aging and age-
related degenerative diseases. Conversely, the cell convenes antioxidant mecha-
nisms to counteract the effect of oxidants; these antioxidantsmay remove oxidants
either in a highly specific manner as in the case of superoxide dismutases or in a
less specific manner (for example, small molecules such as vitamin E, vitamin C,
and glutathione). Oxidative stress is classically defined as an imbalance between
oxidants and antioxidants.1,2 This concept of oxidative stress entails a global view
of, for example, thiol/disulfide balance –a major determinant of the cell redox
state-and fails to recognize discrete redox pathways. Based on this, Jones3 pro-
vided a new definition of oxidative stress as a disruption of redox signaling and
control, in essence, a mechanistic concept. This is important, for redox regulation
of cell signaling occurs in discreet cellular regions that respond differently to
oxidative and/or nitrosative stress situations. More recently, Sies and Jones
introduced a new definition of oxidative stress in the Encyclopedia of Stress as an
imbalance between oxidants and antioxidants in favor of the oxidants, leading
to a disruption of redox signaling and control and/or molecular damage.4
