Autor: |
Mantle D; Pharma Nord (UK) Ltd., Morpeth NE61 2DB, UK., Dewsbury M; School of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool L3 3AF, UK., Hargreaves IP; School of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool L3 3AF, UK. |
Jazyk: |
angličtina |
Zdroj: |
International journal of molecular sciences [Int J Mol Sci] 2024 Jun 20; Vol. 25 (12). Date of Electronic Publication: 2024 Jun 20. |
DOI: |
10.3390/ijms25126765 |
Abstrakt: |
Coenzyme Q10 (CoQ10) plays a key role in many aspects of cellular metabolism. For CoQ10 to function normally, continual interconversion between its oxidised (ubiquinone) and reduced (ubiquinol) forms is required. Given the central importance of this ubiquinone-ubiquinol redox cycle, this article reviews what is currently known about this process and the implications for clinical practice. In mitochondria, ubiquinone is reduced to ubiquinol by Complex I or II, Complex III (the Q cycle) re-oxidises ubiquinol to ubiquinone, and extra-mitochondrial oxidoreductase enzymes participate in the ubiquinone-ubiquinol redox cycle. In clinical terms, the outcome of deficiencies in various components associated with the ubiquinone-ubiquinol redox cycle is reviewed, with a particular focus on the potential clinical benefits of CoQ10 and selenium co-supplementation. |
Databáze: |
MEDLINE |
Externí odkaz: |
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