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Non-Wilsonian copper toxicity: more questions than answers
  1. Lizelle Nagel
  1. Chemical Pathology, University of Pretoria, Faculty of Health Sciences, Pretoria, Gauteng, South Africa
  1. Correspondence to Dr Lizelle Nagel, Chemical Pathology, University of Pretoria Faculty of Health Sciences, Pretoria 0031, South Africa; lizelle.nagel{at}nhls.ac.za

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Copper is an essential redox cofactor and enabler of protein function through electron transfer. The daily requirement is 1 mg; most diets supply 1–5 mg/day with drinking water contributing 6%–13%.1 2 Regulatory limits for drinking water range from 1 mg/L to 3 mg/L. Other sources include contaminated drinking water, copper cookware, intrauterine devices, dietary supplements, fungicides and pesticides. Occupational exposure occurs in plumbers and industrial workers (welders, machinists, smelters, steel production, municipal incinerators).

Free copper causes oxidative damage to cellular organelles, lipids, proteins, carbohydrates and nucleic acids.2 3 Copper homeostasis is tightly regulated to prevent toxicity; plasma copper is extensively ceruloplasmin bound (95%) and intracellular copper is sequestered by cuproproteins …

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Footnotes

  • Handling editor Tahir S Pillay.

  • Contributors Concept, drafting and writing done by LN.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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