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Mitochondrial complex I is deficient in renal oncocytomas
Helene Simonnet1, Jocelyne Demont, Kathy Pfeiffer
1CGMC (Center of Molecular and Cell Genetics), Unit 5534 of the CNRS and the University Lyon 1 Claude Bernard, Villeurbanne, France. simonnet@univ-lyon1.fr
Carcinogenesis
|July 8, 2003
Summary
Renal oncocytomas show a specific decrease in mitochondrial complex I, unlike malignant tumors. This deficiency may drive increased mitochondria and impaired ATP production in these benign kidney tumors.
Area of Science:
- Nephrology
- Mitochondrial Biology
- Oncology
Background:
- Renal oncocytomas are benign tumors with increased mitochondria, but the functionality of their oxidative phosphorylation (OXPHOS) system is unclear.
- Previous studies noted increased mitochondrial DNA and OXPHOS complex activity, yet functional assessment was lacking.
Purpose of the Study:
- To investigate the functional status of mitochondrial complex I in renal oncocytomas.
- To differentiate mitochondrial alterations in oncocytomas from those in malignant renal tumors.
Main Methods:
- Analysis of NADH dehydrogenase activity and protein content of mitochondrial complex I in oncocytomas.
- Comparison of complex I alterations in oncocytomas with those in malignant renal tumors.
- Assessment of complex I activity in peritumoral tissue.
Main Results:
- Renal oncocytomas exhibit a specific decrease in mitochondrial complex I (NADH dehydrogenase) activity and protein content.
- In contrast, malignant renal tumors show a parallel decrease in all respiratory chain complexes.
- Complex I activity is also moderately reduced in tissue adjacent to oncocytomas.
Conclusions:
- Complex I deficiency is a potential early event in oncocytoma development, triggering compensatory mitochondrial biogenesis.
- Oncocytoma represents a third type of benign tumor linked to impaired mitochondrial ATP production.
- The findings suggest oncocytomas arise from at least two sequential alterations affecting the mitochondrial respiratory chain.