Copper Investigating

Case Study

Co-authors:

zak, micky

Corresponding author:

Mike

Abstract:

Although copper (Cu) is recognized as an essential trace element, uncertainties remain regarding Cu reference values for humans, as illustrated by discrepancies between recommendations issued by different national authorities. This review examines human studies published since 1990 on relationships between Cu intake, Cu balance, biomarkers of Cu status, and health. It points out several gaps and unresolved issues which make it difficult to assess Cu requirements. Results from balance studies suggest that daily intakes below 0.8 mg/day lead to net Cu losses, while net gains are consistently observed above 2.4 mg/day.

Keywords: Research Institutes

Description:

Copper (Cu) is an essential trace element in both humans and animals. Needed only in trace amounts, the human body contains approximately 100 mg Cu. As a transition metal, it is a cofactor of many redox enzymes, Ceruloplasmin being the most abundant Cu-dependent ferroxidase enzyme with a Cu-dependent oxidation activity. Beyond its role in iron metabolism, the need for Cu also derives from its involvement in a myriad of biological processes, including antioxidant defense, neuropeptide synthesis and immune function [1], [2]. As a consequence, the wide range of clinical features resulting from perturbations in the activities of cuproenzymes [3] means that although severe Cu deficiency is relatively straightforward to diagnose, identifying marginal deficiency is somewhat problematic. Dietary Cu deficiency can result in adverse consequences throughout the life span. In utero, Cu deficiency may result in impaired development of the cardiovascular system, bone malformation and ongoing neurologic and immunologic abnormalities into infancy and beyond [4], [5]. In adulthood, prolonged marginal Cu deficiency has been associated with alterations in cholesterol metabolism [6], [7].

Though an essential micronutrient for man, Cu is toxic at high levels. An overload of this metal easily leads to Fenton-type redox reactions, resulting in oxidative cell damage and cell death. However, Cu toxicity as a result of dietary excess is generally not considered a widespread health concern, probably as a result of the homeostatic mechanisms controlling Cu absorption and excretion [8].

Dietary reference values for Cu were established for the French population more than a decade ago. Because of the lack of data on Cu metabolism, dietary reference values have been based on data from dietary surveys and balance studies.

The French population reference intakes (ANC—apports nutritionnels conseillés) for Cu are presented in Table 1, along with those established in other countries.

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