title: Hohenheim consensus workshop: copper.
abstract: Copper (Cu) is an essential trace element with many physiological functions. Homeostatic mechanisms exist to allow Cu to act as a cofactor in enzymatic processes and to prevent accumulation of Cu to toxic levels. The aim of this commentary is to better understand the role of dietary Cu supply in deficiency and under physiological and pathological conditions. The essentiality of Cu can be attributed to its role as a cofactor in a number of enzymes that are involved in the defence against oxidative stress. Cu, however, has a second face, that of a toxic compound as it is observed with accumulating evidence in hepatic, neurodegenerative and cardiovascular diseases. The destructive potential of Cu can be attributed to inherent physico-chemical properties. The main property is its ability to take part in Fenton-like reactions in which the highly reactive and extremely deleterious hydroxyl radical is formed. Diseases caused by dietary Cu overload could be based on a genetic predisposition. Thus, an assessment of risk-groups, such as infants with impaired mechanisms of Cu homeostasis regarding detoxification, is of special interest, as their Cu intake with resuspended formula milk may be very high. This implies the need for reliable diagnostic markers to determine the Cu status. These topics were introduced at the workshop by the participants followed by extensive group discussion. The consensus statements were agreed on by all members. One of the conclusions is that a re-assessment of published data is necessary and future research is required.
authors.affiliation: Walther-Straub-Institut für Pharmakologie und Toxikologie der LMU, München, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Schümann
authors.forename: H G
authors.initials: HG
authors.lastname: Classen
authors.forename: H H
authors.initials: HH
authors.lastname: Dieter
authors.forename: J
authors.initials: J
authors.lastname: König
authors.forename: G
authors.initials: G
authors.lastname: Multhaup
authors.forename: M
authors.initials: M
authors.lastname: Rükgauer
authors.forename: K H
authors.initials: KH
authors.lastname: Summer
authors.forename: J
authors.initials: J
authors.lastname: Bernhardt
authors.forename: H K
authors.initials: HK
authors.lastname: Biesalski
mesh_terms: D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology*; D003300:Copper / Q000009:adverse effects / Q000172:deficiency / Q000493:pharmacokinetics / Q000502:physiology; D020022:Genetic Predisposition to Disease; D006706:Homeostasis; D006801:Humans; D017665:Hydroxyl Radical; D007408:Intestinal Absorption; D019636:Neurodegenerative Diseases / Q000097:blood / Q000209:etiology*; D009751:Nutritional Requirements; D009752:Nutritional Status; D009753:Nutritive Value; D018384:Oxidative Stress; D012307:Risk Factors
chemical_list: D017665:Hydroxyl Radical; D003300:Copper