Although copper is an essential micronutrient normally subject to effe
ctive homeostatic control, excess dietary intakes can in some circumst
ances be toxic. Susceptibility to copper toxicosis depends, however, o
n many factors, including species, genetics, age, and diet. This appea
rs to reflect not only variations in the efficiency of the absorption
and excretion of copper but also differences in the intake of other he
patotoxic or protective factors, differences in the cellular distribut
ion of copper, and differences in the expression of specific copper tr
ansport and storage proteins. Many of the toxic effects of copper, suc
h as increased lipid peroxidation in cell membranes and DNA damage, ar
e related to its role in the generation of oxygen free radicals.