Copper is an essential micronutrient for most living organisms, serving as a redox-active cofactor for important enzymes such as the terminal respiratory oxidases and superoxide dismutase. However, in excess copper can be extremely toxic, due in part to this same redox-activity by which copper ions can catalyse the production of deleterious reactive oxygen species (ROS), and also due to its propensity to form extremely stable complexes with cellular components. In recent decades, much has been learned about how organisms acquire, handle, distribute, store, sense and export copper ions, collectively termed copper homeostasis. Yet, despite this progress in our understanding of the molecular bases of copper homeostasis, the molecular mechanisms by which unregulated concentrations of copper ions kill cells remain largely unknown. This question has gained importance in recent years with the recognition that copper, both as metal salts and as solid metal surfaces, is an attractive antimicrobial.
In a world of decreasing efficacy of traditional antibiotics, together with the recognition that prevention of infection is better than cure, such antimicrobial substances and ‘selfsanitising’ surfaces hold much appeal. As with any new antimicrobial, it is important that its mechanism of action is defined prior to widespread adoption, primarily to assess the risk of spontaneous resistance emerging amongst the ‘wild’
microbial population. In this review, we first summarise our current understanding of microbial copper homeostasis, then review what is known of the mechanisms by which copper kills cells. Finally, we look at the current and potential applications of copper toxicity, in both the medical field and commercial activities.
Keywords copper; copper homeostasis; copper toxicity; antimicrobial copper.
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