Copper Toxicity
- PMID: 32491388
- Bookshelf ID: NBK557456
Copper Toxicity
Excerpt
Copper is a trace element (minerals required in amounts of 1 to 100 mg/day by adults) found in high concentrations in the brain, liver, and kidneys. However, because of their size, bone and muscle contain more than half of the copper in the body. Copper is bound to ceruloplasmin in the liver, which transports the copper from the liver to the peripheral tissues. Approximately 50% of copper is excreted in the bile, while the remaining half is excreted through other gastrointestinal secretions. As such, the gastrointestinal tract is the major regulator of copper homeostasis.
While copper is required as an important catalytic cofactor in redox chemistry for many proteins, when present in excess, free copper ions can cause damage to cellular components. A delicate balance between the uptake and efflux of copper ions determines the amount of cellular copper. Excess copper induces not only oxidative stress but also DNA damage and reduced cell proliferation. Ingestion of more than 1 g of copper sulfate results in symptoms of toxicity. Copper toxicosis can be classified as primary when it results from an inherited metabolic defect and secondary when it results from high intake, increased absorption, or reduced excretion due to underlying pathologic processes. Copper toxicity (copperidus) can be caused by consuming acidic foods cooked in uncoated copper cookware or exposure to excess copper in drinking water or other environmental sources.
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References
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- Mason KE. A conspectus of research on copper metabolism and requirements of man. J Nutr. 1979 Nov;109(11):1979-2066. - PubMed
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- Oe S, Miyagawa K, Honma Y, Harada M. Copper induces hepatocyte injury due to the endoplasmic reticulum stress in cultured cells and patients with Wilson disease. Exp Cell Res. 2016 Sep 10;347(1):192-200. - PubMed
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