Platelets Mitochondrial Function Depends on Coenzyme Q10 Concentration in Human Young, Not in Elderly Subjects

Ageing is characterized by a progressive decline in the physiological functions of various organs. Mitochondrial alterations occurring in senescence. Antioxidants, including coenzyme Q10 concentration, fall with ageing and contribute to enhanced oxidative stress age-related diseases. The impairment of platelet mitochondrial function occurs in a broad spectrum of diseases. The aim of this study was to evaluate mitochondrial function in platelets in elderly and young human controls and correlate it with a concentration of coenzyme Q10. Platelets mitochondrial function was determined by the use of High-Resolution Respirometry method.We did not find significantly decreased platelet mitochondrial function in elderly subjects. Dependence of platelets mitochondrial respiratory chain function and ATP production at Complex I on a concentration of coenzyme Q10 in platelets and whole blood in young not in elderly human volunteers was documented. This dependence was not found for Complex II in any group. Platelet mitochondrial coenzyme Q10 concentration was insufficient for improving platelet mitochondrial function in elderly human subjects. Recommending supplementation with coenzyme Q10 in elderly and aged humans is waranted.High-Resolution Respirometry method offers a perspective to diagnose mitochondrial energy metabolism which might be useful for further studies in patients with mitochondrial disorders. Our results could contribute to the explanation of platelets mitochondrial function in elderly and aged human subjects

Platelet Mitochondrial Bioenergetics Reprogramming in Patients with Urothelial Carcinoma

Mitochondrial bioenergetics reprogramming is an essential response of cells to stress. Platelets, an accessible source of mitochondria, have a crucial role in cancer development; however, the platelet mitochondrial function has not been studied in urothelial carcinoma (UC) patients. A total of 15 patients with UC and 15 healthy controls were included in the study. Parameters of platelet mitochondrial respiration were evaluated using the high-resolution respirometry method, and the selected antioxidant levels were determined by HPLC. In addition, oxidative stress was evaluated by the thiobarbituric acid reactive substances (TBARS) concentration in plasma. We demonstrated deficient platelet mitochondrial respiratory chain functions, oxidative phosphorylation (OXPHOS), and electron transfer (ET) capacity with complex I (CI)-linked substrates, and reduced the endogenous platelet coenzyme Q10 (CoQ10) concentration in UC patients. The activity of citrate synthase was decreased in UC patients vs. controls (p = 0.0191). γ-tocopherol, α-tocopherol in platelets, and β-carotene in plasma were significantly lower in UC patients (p = 0.0019; p = 0.02; p = 0.0387, respectively), whereas the plasma concentration of TBARS was increased (p = 0.0022) vs. controls. The changes in platelet mitochondrial bioenergetics are consistent with cell metabolism reprogramming in UC patients. We suppose that increased oxidative stress, decreased OXPHOS, and a reduced platelet endogenous CoQ10 level can contribute to the reprogramming of platelet mitochondrial OXPHOS toward the activation of glycolysis. The impaired mitochondrial function can contribute to increased oxidative stress by triggering the reverse electron transport from the CoQ10 cycle (Q-junction) to CI