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Coordination chemistry of mitochondrial copper metalloenzymes: exploring implications for copper dyshomeostasis in cell death

  • 작성자

    Jiyeon Han
  • 작성일자

    2023-12-21
  • 조회수

    582
Name: Jiyeon Han ( jiyeonhan@uoa.ac.kr )
2022.9-presentAssistant Professor, Department of Applied Chemistry, University of Seoul
2022.3-2022.8Postdoctoral Scholar, Korea Advanced Institute Science and Technology (KAIST), Daejeon, Korea
2018.9-2022.2Ph.D., Department of Chemistry, Korea Advanced Institute Science and Technology (KAIST), Daejeon, Korea
2016.9-2018.2M.S., Department of Chemistry, Ulsan National Institute of Science and Technology (UNIST), Daejeon, Korea
2012.3-2016.8B.S., Department of Chemistry, Ulsan National Institute of Science and Technology (UNIST), Daejeon, Korea

Coordination chemistry of mitochondrial copper metalloenzymes: exploring implications for copper dyshomeostasis in cell death

Mitochondria, fundamental cellular organelles that govern energy metabolism, hold a pivotal role in cellular vitality. While consuming dioxygen to produce adenosine triphosphate (ATP), the electron transfer process within mitochondria can engender the formation of reactive oxygen species that exert dual roles in endothelial homeostatic signaling and oxidative stress. In the context of the intricate electron transfer process, several metal ions that include copper, iron, zinc, and manganese serve as crucial cofactors in mitochondrial metalloenzymes to mediate the synthesis of ATP and antioxidant defense. In this mini review, we provide a comprehensive understanding of the coordination chemistry of mitochondrial cuproenzymes. In detail, cytochrome c oxidase (CcO) reduces dioxygen to water coupled with proton pumping to generate an electrochemical gradient, while superoxide dismutase 1 (SOD1) functions in detoxifying superoxide into hydrogen peroxide. With an emphasis on the catalytic reactions of the copper metalloenzymes and insights into their ligand environment, we also outline the metalation process of these enzymes throughout the copper trafficking system. The impairment of copper homeostasis can trigger mitochondrial dysfunction, and potentially lead to the development of copper-related disorders. We describe the current knowledge regarding copper-mediated toxicity mechanisms, thereby shedding light on prospective therapeutic strategies for pathologies intertwined with copper dyshomeostasis.


BMB Rep. 2023 Nov;56(11):575-583. doi: 10.5483/BMBRep.2023-0172
https://pubmed.ncbi.nlm.nih.gov/37915136/