The role and mechanisms of oxidative stress and of antioxidant
molecules in patients with cardiovascular disease have been the subject of
intense experimental and clinical research recently. Rapid accumulation of
new knowledge in this field since the beginning of the 2V^ century amply
justifies this second edition of the book Antioxidants & Cardiovascular
Disease.
The generation of reactive oxygen species (ROS) is an unavoidable
consequence of life in an aerobic environment. Cells produce ROS as part of
their general metabolic activity. ROS are a family of molecules derived from
oxygen, and characterized by their high chemical reactivity and ability to act
as oxidants. ROS encompass free radicals (species containing highly reactive
unpaired electrons) such as superoxide (02-) and hydroxyl radicals (OH), as
well as other molecules such as hydrogen peroxide (H202) and peroxynitrite
(ONOO), which are not free radicals, but can also act as oxidizing agents in
biological systems. Under physiological conditions, there is a balance
between ROS generation and the activity of enzymatic (superoxide
dismutase, catalase, glutathione peroxidase) and non-enzymatic (glutathione,
alpha-tocopherol, ascorbate, thioredoxin) antioxidant defences that decrease
ROS concentrations. ROS are normally produced in low concentrations and
exert important physiological functions in the vessel wall. However,
increased production of ROS or decreased antioxidant defences result in
excess production of ROS, a condition referred to as oxidative stress.
Oxidative stress can lead to free radical-induced oxidation and damage to
bio-molecules such as lipids, DNA and proteins. ROS-mediated cellular
damage has been associated with the pathogenesis of many diseases including Alzheimer's disease, rheumatoid arthritis, asthma, diabetes and
especially cardiovascular disease.
