Protective effect of vitamin E on sperm motility and oxidative stress in valproic acid treated rats |
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| Institution: | 1. Department of Physiology and Pharmacology, Federal University of Santa Maria (UFSM), Santa Maria, RS, 97105-900, Brazil;2. Laboratory of Biotechnology and Animal Reproduction - BioRep, Federal University of Santa Maria (UFSM), Santa Maria, RS, 97105-900, Brazil;3. Department of Morphology, Federal University of Santa Catarina (UFSC), Florianópolis, SC 88040-900, Brazil;1. Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran;2. Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran;3. Department of Anatomy, School of Medicine, Tehran University of Medical Science, Tehran, Iran;4. Alzahra Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran;1. Laboratory of Biosignaling & Therapeutics, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium;2. Department of Chemistry and Biochemistry, University of Arizona, Tucson, AZ 85718, USA;3. Laboratory of Structural Neurobiology, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium;4. Protein Phosphorylation & Proteomics Lab, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium;5. Biomolecular Architecture, Department of Chemistry, KU Leuven, Leuven, Belgium;1. Institute of Physical Chemistry and Chemical Physics, Slovak University of Technology in Bratislava, Radlinského 9, SK-812 37 Bratislava, Slovak Republic;2. Department of Chemistry, University of SS. Cyril and Methodius, J. Herdu 2, SK-917 01 Trnava, Slovak Republic |
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| Abstract: | Long-term administration of valproic acid (VPA) is known to promote reproductive impairment mediated by increase in testicular oxidative stress. Vitamin E (VitE) is a lipophilic antioxidant known to be essential for mammalian spermatogenesis. However, the capacity of this vitamin to abrogate the VPA-mediated oxidative stress has not yet been assessed. In the current study, we evaluated the protective effect of VitE on functional abnormalities related to VPA-induced oxidative stress in the male reproductive system. VPA (400 mg kg?1) was administered by gavage and VitE (50 mg kg?1) intraperitoneally to male Wistar rats for 28 days. Analysis of spermatozoa from the cauda epididymides was performed. The testes and epididymides were collected for measurement of oxidative stress biomarkers. Treatment with VPA induced a decrease in sperm motility accompanied by an increase in oxidative damage to lipids and proteins, depletion of reduced glutathione and a decrease in total reactive antioxidant potential on testes and epididymides. Co-administration of VitE restored the antioxidant potential and prevented oxidative damage on testes and epididymides, restoring sperm motility. Thus, VitE protects the reproductive system from the VPA-induced damage, suggesting that it may be a useful compound to minimize the reproductive impairment in patients requiring long-term treatment with VPA. |
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| Keywords: | Sodium valproate Alpha-tocopherol Reproductive toxicity Oxidative damage Antioxidants |
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