There is growing evidence that oxidative stress may represent one of the agents involved in the initiation and/or progression of many human diseases including atherosclerosis, postischemic reperfusion injury, inflammation, aging, and neurodegenerative pathologies (Parkinson’s and Alzheimer’s diseases). In addition, several experimental results link the overproduction of ROS to biological damage. ROS, in fact, are able to chemically alter virtually all the major classes of biomolecules (proteins, nucleic acids, and lipids). Like other aerobic organisms, humans have evolved a variety of mechanisms to protect themselves from the potentially deleterious effects of ROS; nevertheless, oxidative stress occurs when the generation of free radicals exceeds the capacity of a cell to defend or repair itself.