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.