# In Vitro Antioxidant Effects of Coenzyme Q10 on Cellular Metabolism in Aged Mesenchymal Stem Cells
## 5 Conclusions  
Our findings suggest that CoQ10 enhances cellular metabolism through its potent antioxidant properties and by modulating membrane stability. It upregulates PPAR activity, facilitating \(\beta\)-oxidation and mitigating oxidative damage, especially in aging cells. CoQ10 shows promise in improving mitochondrial function and enhancing metabolic fitness in both youthful and senescent cells. Supplementation with CoQ10 enhances mitochondrial respiration and efficiency, partially restoring these parameters in aged cells. Additionally, CoQ10 upregulates PPAR and catalase, promoting fatty acid oxidation and reducing oxidative stress, particularly via peroxisomal \(\beta\)-oxidation. The resulting shift in the fatty acid profile may improve cellular membrane rigidity and enzymatic stability, increasing resilience against oxidative damage. However, our current study was focused only on the short-term effects of CoQ10 addition (up to 24 h) The long-term effects of CoQ10 in mitigating age-related oxidative stress, modulating inflammatory processes, and maintaining genomic stability should be investigated, along with biosafety and bioavailabilitystudies. A better understanding of the mechanistic interactions between CoQ10 supplementation, stem cell metabolism, and age-associated cellular alterations could ultimately lead to targeted interventions for age-related pathologies, including cancer. Exploring dose-dependent responses, optimal delivery strategies, and potential synergistic interactions with other compounds will be crucial for a deeper understanding of CoQ10's potential to enhance cellular health, support longevity, and counteract age-related metabolic decline. The following supporting information can be downloaded at: [[https://www.mdpi.com/article/10.3390/app15052783/s1](https://www.mdpi.com/article/10.3390/app15052783/s1)]([https://www.mdpi.com/article/10.3390/app15052783/s1](https://www.mdpi.com/article/10.3390/app15052783/s1)), Figure S1. Coupled and uncoupled respiration of intact cells: Representative Oroboros oxygraphs illustrating the oxygen consumption profile of SHED cells, measured using high-resolution respiratory. The traces display basal respiration, followed by oligomycin-insensitive respiration after the addition of oligomycin to inhibit ATP synthase. Subsequent additions of FCCP reveal the maximal respiratory capacity, while rotenone (Rot) and antimycin A (AmyA) are introduced to selectively inhibit mitochondrial complexes, providing a comprehensive assessment of mitochondrial function; Table S1. Primer sequence for q-PCR analysis; Figure S2. Agarose gel electrophoresis analysis of qPCR products targeting oxidative stress-related genes (PPARy, ACC, SOD, CAT) and sirutin family members (SIRT1, SIRT3, SIRT4, SIRT5, SIRT6, SIRT7); Figure S3. Representative GC-MS chromatogram showcasing the major fatty acid methyl esters (FAMEs) detected in the early passage cell (P5) samples and late passage cell (P16) samples before and following CoQ10 treatement, including lauric acid methyl ester (C12:0), myristic acid methyl ester (C14:0), palmitic acid methyl ester (C16:0), stearic acid methyl ester (C18:0), oleic acid methyl ester (C18:1 cis-9), and elaidic acid methyl ester (C18:1 trans-9). Conceptualization, A.I. and I.-M.C. ; methodology, A.I. ; validation, A.I., I.-M.C. and A.T.L.-G.; formal analysis, A.I., A.T.L.-G., I.-M.C., M.-A.P. and C.L.C. ; investigation, A.I., A.T.L.-G., I.-M.C., M.-A.P., C.L.C. and A.P. ; resources, C.A.T., A.G. and V.P. ; data curation, A.I., A.T.L.-G. and C.A.T. ; writing--original draft preparation, A.I. ; writing--review and editing, A.I., A.T.L.-G. and C.A.T. ; visualization, A.I., A.T.L.-G. and C.A.T. ; supervision, C.A.T., A.G. and V.P. All authors have read and agreed to the published version of the manuscript. This research received no external funding.