Toxic metals (lead,
cadmium,
mercury and
arsenic) are widely found in our environment. Humans are exposed to these metals from numerous sources, including contaminated air, water, soil and food. Recent studies indicate that transition metals act as catalysts in the oxidative reactions of
biological macromolecules therefore the toxicities associated with these metals might be due to oxidative tissue damage. Redox-active metals, such as
iron,
copper and
chromium, undergo redox cycling whereas redox-inactive metals, such as lead,
cadmium,
mercury and others deplete cells' major
antioxidants, particularly
thiol-containing
antioxidants and
enzymes. Either redox-active or redox-inactive metals may cause an increase in production of
reactive oxygen species (ROS) such as
hydroxyl radical (HO.),
superoxide radical (O2.-) or
hydrogen peroxide (H2O2). Enhanced generation of ROS can overwhelm cells' intrinsic
antioxidant defenses, and result in a condition known as "oxidative stress". Cells under oxidative stress display various dysfunctions due to lesions caused by ROS to
lipids,
proteins and
DNA. Consequently, it is suggested that
metal-induced oxidative stress in cells can be partially responsible for the toxic effects of
heavy metals. Several studies are underway to determine the effect of
antioxidant supplementation following
heavy metal exposure. Data suggest that
antioxidants may play an important role in abating some hazards of
heavy metals. In order to prove the importance of using
antioxidants in
heavy metal poisoning, pertinent biochemical mechanisms for
metal-induced oxidative stress should be reviewed.