| Autor: |
Foteini Malli, Fotini Bardaka, Zissis Mamuris, Eugenios Bouzetos, Anna-Maria Psara, Emily Zifa, Maria Fouka, Ourania S. Kotsiou, Zoe Daniil, Helen Panagiotidou, Konstantinos I. Gourgoulianis, Katerina M. Antoniou |
| Rok vydání: |
2018 |
| Předmět: |
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| Zdroj: |
Sarcoidosis and other granulomatous ILD/DPLD. |
| Popis: |
Background: Complex I (NADH-ubiquinone oxidoreductase) is the largest enzyme of the respiratory electron transport chain in mitochondria, central to ATP production, mtDNA protein translation, membrane protein insertion, and stabilization. It is also a major source of reactive oxygen species (ROS). Enhanced ROS production is suggested to play a role in the pathogenesis of sarcoidosis. Previous research by our team identified multiple novel as well as known mutations in mitochondrial transfer RNA genes that were exclusively or predominantly expressed in patients with sarcoidosis, compared to controls (preliminary data). Aim: To evaluate the activity of complex I in blood lymphocytes of patients with sarcoidosis compared to a group of matched healthy controls. Materials and Methods: Peripheral blood lymphocytes were freshly isolated from 23 patients with sarcoidosis and 17 healthy controls, according to the recommended standard protocol for lymphocyte isolation. To evaluate a deficiency of Complex I activity we used a spectrophometric assay measuring rotenone-sensitive NADH oxidation by Complex I. Results: Patients with sarcoidosis had significantly lower complex I activity compared to controls (36.37±14.22 mU/mgr vs. 73.34±27.97 mU/mg, p Conclusion: For the first time, reduced activity of complex I has been detected in sarcoidosis group compared to controls. Our findings indicate that sarcoidosis is closely related to mitochondrial respiratory chain dysfunction. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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