如果没有铜的氧化还原活性，高等真核生物的生命就不可能存在，而且，从字面上看，我们的每一次呼吸都在生化上证明了这一点。然而，为了确保以目标为导向的铜行动，这种依赖付出了相当大的代价。此外，它的吸收、分布以及排泄都是由对过渡金属具有高亲和力的特殊蛋白质执行的。因此，铜酶/转运蛋白的功能障碍（如影响细胞内铜转运蛋白 ATP7B 的遗传性威尔逊病）会带来严重的细胞损伤。这种疾病的一个标志是铜的进行性积累，主要是在肝脏中，但也在大脑中，如果不及时治疗就会致命。这种过量的铜毒性也可能是由于意外摄入或自杀未遂造成的。最近的研究为细胞毒性机制提供了新的线索，并且主要影响细胞内的靶标和过量铜的过程，甚至可以将其用于癌症治疗。此外，目前正在开发新疗法来对抗致命的有毒铜。版权所有 © 2024 作者。由 Elsevier B.V. 出版。保留所有权利。

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.Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.