In vivo and in vitro assessment of brain bioenergetics in aging rats |
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Authors: | Ol’ga Vančová Ladislav Bačiak Svatava Kašparová Jarmila Kucharská Hector H. Palacios Jaromír Horecký Gjumrakch Aliev |
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Affiliation: | 1. Pharmacobiochemical Laboratory, Comenius University School of Medicine, Bratislava, Slovakia;2. Institute of Analytical Chemistry, Slovak Technical University, Bratislava, Slovakia;3. Department of Biology College of Sciences University of Texas at San Antonio, San Antonio, TX, USA;4. Surgical Pathophysiology and Tissue Engineering Center, Slovak Medical University, Bratislava, Slovakia;5. Department of Nutrition and Biochemistry, Faculty of Sciences, Javeriana University, Bogota D.C., Colombia;6. Stress Relief and Memory Training Center, Brooklyn, NY, USA |
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Abstract: | Brain energy disorders can be present in aged men and animals. To this respect, the mitochondrial and free radical theory of aging postulates that age‐associated brain energy disorders are caused by an imbalance between pro‐ and anti‐oxidants that can result in oxidative stress. Our study was designed to investigate brain energy metabolism and the activity of endogenous antioxidants during their lifespan in male Wistar rats. In vivo brain bioenergetics were measured using 31P nuclear magnetic resonance (NMR) spectroscopy and in vitro by polarographic analysis of mitochondrial oxidative phosphorylation. When compared to the young controls, a significant decrease of age‐dependent mitochondrial respiration and adenosine‐3‐phosphate (ATP) production measured in vitro correlated with significant reduction of forward creatine kinase reaction (kfor) and with an increase in phosphocreatine (PCr)/ATP, PCr/Pi and PME/ATP ratio measured in vivo. The levels of enzymatic antioxidants catalase, GPx and GST significantly decreased in the brain tissue as well as in the peripheral blood of aged rats. We suppose that mitochondrial dysfunction and oxidative inactivation of endogenous enzymes may participate in age‐related disorders of brain energy metabolism. |
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Keywords: | aging brain 31P NMR mitochondria OXPHOS antioxidants |
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