Resveratrol preserves mitochondrial function in a human post-mitotic cell model |
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| Institution: | 1. Depto. de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán”, Ciudad de México, Mexico;2. Facultad de Química, Universidad Nacional Autónoma de México, Ciudad de México, Mexico;1. Department of Biomedical Sciences, University of North Dakota, Grand Forks, ND 58202;2. Department of Nutrition and Food Sciences, Texas A&M University, College Station, TX 77843;3. Department of Pathology, University of North Dakota, Grand Forks, ND 58202;4. ND-INBRE Bioinfomatic Core, University of North Dakota, Grand Forks, ND 58202;5. Hubei Cancer Hospital, Wuhan, Hubei 430079, China;6. Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China;7. Campus Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China;8. Department of Pathology, University Medical Center of Princeton, Plainsboro, NJ, USA;9. Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, USA;10. Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA;1. Department of Obstetrics & Gynecology, University of Colorado Anschutz Medical Campus Aurora, CO, USA;2. Division of High-risk Pregnancy, Department of Obstetrics & Gynecology, Mackay Memorial Hospital, Taipei, Taiwan;3. Children''s Health Research Institute, University of Western Ontario, London, ON, Canada;4. Department of Pediatrics and Biochemistry, University of Western Ontario, London, ON, Canada;5. Department of Obstetrics and Gynecology, University of Western Ontario, London, ON, Canada;6. Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA;1. Laboratory of Experimental Physiology, Department of Physiological Sciences, Federal University of Maranhão, São Luís, (MA), Brazil;2. Laboratory of Vascular Biology, Heart Institute of the School of Medicine, University of São Paulo, São Paulo, (SP), Brazil |
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| Abstract: | Dysfunctions caused by genetic defects in the mitochondrial DNA (mtDNA) of humans are called mitochondrial diseases; however, mtDNA mutations are also associated with aging and age-related diseases. Here, we present an original cellular model that allows gathering information on molecules that might contrast or prevent mitochondrial dysfunctions and their related diseases. This model allowed us to show that resveratrol (RSV), a phytochemical present in food, exerts protective effects at low concentrations on resting human fibroblasts carrying dysfunctional respiratory chain Complex I. Cells were maintained both in resting condition, to mimic the high energy demanding post-mitotic tissues (serum absence and gramicidin presence), and under glucose deficiency to push the synthesis of ATP via oxidative phosphorylation. Pre-incubation with RSV prolonged the viability of the fibroblasts exposed to rotenone, a well-known specific inhibitor of the respiratory chain Complex I, and decreased mitochondrial fragmentation. It significantly prevented the oxidative phosphorylation impairment indirectly caused by the rotenone-mediated Complex I inhibition, allowing for an almost complete preservation of the cellular ATP level. Indeed, RSV limited the rotenone-induced reactive oxygen species increase, allowing for the maintenance of a functional mitochondrial membrane potential. These findings indicate the potential usage of resveratrol to prevent or possibly treat many disorders, in which the bioenergetic defects and oxidative stress are the primary (mitochondrial encephalomyopathy), or the secondary (age-related diseases) causes of the pathology; and to also assist cell senescence during aging. |
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