Deadly excess copper

• Published in: Redox biology Vol. 75; p. 103256
• Main Authors: Sailer, Judith, Nagel, Judith, Akdogan, Banu, Jauch, Adrian T., Engler, Jonas, Knolle, Percy A., Zischka, Hans
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.09.2024; Elsevier
• Subjects: Acute copper toxicity; Invited Review; Mitochondria; Wilson disease; Wilson disease; Mitochondria; Acute copper toxicity
• ISSN: 2213-2317; 2213-2317
• DOI: 10.1016/j.redox.2024.103256

Higher eukaryotes’ life is impossible without copper redox activity and, literally, every breath we take biochemically demonstrates this. However, this dependence comes at a considerable price to ensure target-oriented copper action. Thereto its uptake, distribution but also excretion are executed by specialized proteins with high affinity for the transition metal. Consequently, malfunction of copper enzymes/transporters, as is the case in hereditary Wilson disease that affects the intracellular copper transporter ATP7B, comes with serious cellular damage. One hallmark of this disease is the progressive copper accumulation, primarily in liver but also brain that becomes deadly if left untreated. Such excess copper toxicity may also result from accidental ingestion or attempted suicide. Recent research has shed new light into the cell-toxic mechanisms and primarily affected intracellular targets and processes of such excess copper that may even be exploited with respect to cancer therapy. Moreover, new therapies are currently under development to fight against deadly toxic copper.