Mitochondrial function is differentially affected upon oxidative stress |
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| Institution: | 1. Center for Neuroscience of Coimbra, University of Coimbra, Portugal;2. Faculty of Medicine of Coimbra, University of Coimbra, Coimbra, Portugal;1. Physics Department, University of Lucknow, Lucknow 226 007, India;2. School of Pharmaceutical Sciences, Hebei Medical University, Shijiazhuang 050017, China;1. Department of Conservative Dentistry, Seoul National University Dental Hospital, School of Dentistry, Dental Research Institute, Seoul National University, Jongro-Gu, Seoul, Korea;2. Department of Maxillofacial Tissue Regeneration, School of Dentistry, Kyung Hee University, Hoegi-dong, Dongdaemun-gu, Seoul, Korea;3. Department of Oral Histology–Developmental Biology and Dental Research Institute, School of Dentistry, Seoul National University, Seoul, Korea;1. Department of Chemistry, Arignar Anna Govt Arts & Science College, Karaikal 609 605, India;2. Research and Development Centre, Bharathiar University, Coimbatore, 641 046, India;3. Institute of Low Temperature and Structure Research, Polish Academy of Sciences, 50–950, Wroclaw 2, P.O. Box 1410, Poland;4. School Sciences and Humanities, Vel Tech University, Chennai, 600 062, India;1. Department of Stomatology, The Second Xiangya Hospital, Central South University, Changsha, China;2. Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha, China;1. Department of Chemistry, National Institute of Technology, Rourkela 769008, Odisha, India;2. Department of Chemistry, Western Michigan University, Kalamazoo, MI 49008, USA;3. Institute of Physics, University of Neuchâtel, Rue Emile-Argand 11, CH-2000 Neuchâtel, Switzerland;4. Department of Life Science, National Institute of Technology, Rourkela 769008, Odisha, India;5. Department of Inorganic Chemistry, IACS Kolkata, Kolkata 700032, West Bengal, India |
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| Abstract: | The mechanisms that lead to mitochondrial damage under oxidative stress conditions were examined in synaptosomes treated with ascorbate/iron. A loss of membrane integrity, evaluated by electron microscopy and by LDH leakage, was observed in peroxidized synaptosomes and it was prevented by pre-incubation with vitamin E (150 μM) and idebenone (50 μM). ATP levels decreased, in synaptosomes exposed to ascorbate/iron, as compared to controls. NADH-ubiquinone oxidoreductase (Cx I) and cytochrome c oxidase (Cx IV) activities were unchanged after ascorbate/iron treatment, whereas succinate-ubiquinone oxidoreductase (Cx II), ubiquinol cytochrome c reductase (Cx III) and ATP-synthase (Cx V) activities were reduced by 55%, 40%, and 55%, respectively. The decrease of complex II and ATP-synthase activities was prevented by reduced glutathione (GSH), whereas the other antioxidants tested (vitamin E and idebenone) were ineffective. However, vitamin E, idebenone and GSH prevented the reduction of complex III activity observed in synaptosomes treated with ascorbate/iron. GSH protective effect suggests that the oxidation of protein SH-groups is involved in the inhibition of complexes II, III and V activity, whereas vitamin E and idebenone protection suggests that membrane lipid peroxidation is also involved in the reduction of complex III activity. These results may indicate that the inhibition of the mitochondrial respiratory chain enzymatic complexes, that are differentially affected by oxidative stress, can be recovered by specific antioxidants. |
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