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.

Antioxidant Activity of Sulfur and Selenium: A Review of Reactive Oxygen Species Scavenging, Glutathione Peroxidase, and Metal-Binding Antioxidant Mechanisms

“…Although transition metal ions are essential, they must also be regulated due to their potential toxic effects. Metal toxicity due to mis-regulation of homeostasis results in increased oxidative stress due to ROS generation and has been implicated in diseases such as hemochromatosis, anemia, Wilson's and Menkes diseases, diabetes, ALS, cancer, and inflammatory and neurodegenerative diseases [5,[64][65][66][67][68][69][70]. Cells employ multiple pathways to maintain metal homeostasis [71]; however, metal-mediated ROS generation and subsequent cellular damage still occur.…”

Copper-catalyzed Protein Oxidation and Its Modulation by Carbon Dioxide

“…myeloperoxidasemediated oxidations) of sulfhydryl groups (1) or copper-mediated oxidative damage to biomolecules (2). Indeed, the occurrence of loosely bound copper ions has been reported for a number of clinical samples from pathological conditions involving oxidative stress and inflammation, such as in Wilson disease plasma during an episode of fulminant hepatitis, rheumatoid arthritis synovial fluid, Parkinson disease cerebrospinal fluid, senile plaques of Alzheimer disease (3,4), and blood, aqueous humor, and vitreous bodies of diabetes mellitus patients (5). Copper-catalyzed oxidations and alteration of tissue components have been implicated in organ damage in many of these pathologies (2-4, 6 -11), and in most of them, a sitespecific mechanism of oxidative damage to proteins and other biomolecules has been demonstrated (3,7,(11)(12)(13)(14)(15).…”

Attenuation of Zn-Induced Acute Pancreatitis in Wistar Rat Fed on Cu- and Mg- Enriched Modified Poultry % MathType!Translator!2!1!AMS LaTeX.tdl!TeX -- AMS-LaTeX!% MathType!MTEF!2!1!+-% feaaeaart1ev0aaatCvAUfeBSjuyZL2yd9gzLbvyNv2CaerbuLwBLn% hiov2DGi1BTfMBaeXatLxBI9gBaerbd9wDYLwzYbItLDharqqtubsr% 4rNCHbGeaGqiVu0Je9sqqrpepC0xbbL8F4rqqrFfpeea0xe9Lq-Jc9% vqaqpepm0xbba9pwe9Q8fs0-yqaqpepae9pg0FirpepeKkFr0xfr-x% fr-xb9adbaqaaeGaciGaaiaabeqaamaabaabaaGcbaacbeGaa8xrai% aa-DgacaWFNbWaaWbaaSqabeaaiiqacqGFOoqwaaaaaa!3

“…Zn, Cu, and Se play vital roles as structural catalytic components of metalloenzyme in antioxidant defense system such as superoxide dismutase (SOD), catalase, and glutathione peroxidase [1,42]. The higher Zn supplementation in the present study resulted in Cu reduction in the tissues as evidenced by reduced level of Cu in the liver in our previous study, leading to focal hypertrophy of acinar cells of the pancreas accompanied by vacuolization of cytoplasm and ER in groups II and III rats (Figs.…”