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Abstract
Copper (Cu) is an integral part of many important enzymes involved in a number of
vital biological processes. Although normally bound to proteins, Cu may be released
and become free to catalyze the formation of highly reactive hydroxyl radicals. Data
obtained from in vitro and cell culture studies are largely supportive of Cu's capacity
to initiate oxidative damage and interfere with important cellular events. Oxidative
damage has been linked to chronic Cu-overload and/or exposure to excess Cu caused
by accidents, occupational hazards, and environmental contamination. Additionally,
Cu-induced oxidative damage has been implicated in disorders associated with abnormal
Cu metabolism and neurodegenerative changes. Interestingly, a deficiency in dietary
Cu also increases cellular susceptibility to oxidative damage. A number of nutrients
have been shown to interact with Cu and alter its cellular effects. Vitamin E is generally
protective against Cu-induced oxidative damage. While most in vitro or cell culture
studies show that ascorbic acid aggravates Cu-induced oxidative damage, results obtained
from available animal studies suggest that the compound is protective. High intakes
of ascorbic acid and zinc may provide protection against Cu toxicity by preventing
excess Cu uptake. Zinc also removes Cu from its binding site, where it may cause free
radical formation. Beta-carotene, alpha-lipoic acid and polyphenols have also been
shown to attenuate Cu-induced oxidative damage. Further studies are needed to better
understand the cellular effects of this essential, but potentially toxic, trace mineral
and its functional interaction with other nutrients.