Many findings on the oxidative damage to various biological macromolecules
caused by exposure to Pb or Cd suggest that even though
these metals are non-redox, they can cause disturbances in oxidative
status that can significantly contribute to many adverse effects
of these two toxic metals. Lipid peroxidation in red blood cell membranes
as a consequence of Pb-induced oxidative stress leads to
hemolysis and contributes to Pb-induced anemia (Flora et al., 2012).
Studies conducted on three different animal species with different
dose levels of Cd and via different routes of exposure provide a substantial
body of evidence that confirms oxidative stress as one of
the important mechanisms of Cd toxicity, with liver as a critical target
organ of acute exposure and kidneys as critical target organ of prolonged
exposure to Cd (Matovic´ et al., 2013).