Abstract

Introduction: Cancer patients' fatigue is one of the most common symptoms with the greatest negative impact on quality of life, but it is also one of the least understood. The goal of this study was to look into changes in mitochondrial function and cancer-related fatigue in patients with non-metastatic prostate cancer who were receiving localised radiation therapy (XRT). Methods: We proposed a mitochondrial bioenergetic mechanism of radiation-induced fatigue that links impaired oxidative phosphorylation (OXPHOS) via a complex III defect and adenosine triphosphate (ATP) depletion as a result of XRT. Integrated mitochondrial function was measured as mitochondrial OXPHOS from peripheral blood mononuclear cells (PBMCs) of patients with prostate cancer. Fatigue was measured using the revised Piper Fatigue Scale. Data were collected before (day 0) and at day 21 of XRT. Results: Fatigue symptom intensified in 15 patients with prostate cancer at day 21 of XRT (p < 0.05). Mitochondrial OXPHOS complex III-linked and uncoupled complex III rates in PBMCs at day 21 during XRT were considerably lower than before XRT (p < 0.05). Additionally, in individuals undergoing XRT, a higher fatigue score was connected to a lower OXPHOS complex III-linked respiration rate. Conclusion:  At day 21 of XRT, a defect in oxidation starting at complex III in PBMC mitochondria was discovered in 15 prostate cancer patients. Complex III is a potential target for pharmacological and, in particular, nutraceutical interventions, such as coenzyme Q10, in the development of CRF nursing interventions.

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