Effects of methylglyoxal and pyridoxamine in rat brain mitochondria bioenergetics and oxidative status
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- 作者：Susana Cardoso ; Cristina Carvalho…
- 关键词：Brain mitochondria ; Methylglyoxal ; Oxidative stress ; Pyridoxamine
- 刊名：Journal of Bioenergetics and Biomembranes
- 出版年：2014
- 出版时间：October 2014
- 年：2014
- 卷：46
- 期：5
- 页码：347-355
- 全文大小：413 KB
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Cristina Carvalho (1)
Ricardo Marinho (2)
Anabel Sim?es (1)
Cristina M. Sena (3) (4)
Paulo Matafome (3) (4)
Maria S. Santos (1) (5)
Raquel M. Sei?a (3) (4)
Paula I. Moreira (1) (3)
1. CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
2. Faculty of Medicine, University of Coimbra, Coimbra, Portugal
3. Laboratory of Physiology-Faculty of Medicine, University of Coimbra, 3000-354, Coimbra, Portugal
4. IBILI-Institute for Biomedical Imaging and Life Sciences, Faculty of Medicine, University of Coimbra, Coimbra, Portugal
5. Department of Life Sciences-Faculty of Sciences and Technology, University of Coimbra, Coimbra, Portugal - ISSN：1573-6881
文摘
Advanced glycation end products (AGEs) and methylglyoxal (MG), an important intermediate in AGEs synthesis, are thought to contribute to protein aging and to the pathogenesis of age-and diabetes-associated complications. This study was intended to investigate brain mitochondria bioenergetics and oxidative status of rats previously exposed to chronic treatment with MG and/or with pyridoxamine (PM), a glycation inhibitor. Brain mitochondrial fractions were obtained and several parameters were analyzed: respiratory chain [states 3 and 4 of respiration, respiratory control ratio (RCR), and ADP/O index] and phosphorylation system [transmembrane potential (ΔΨm), ADP-induced depolarization, repolarization lag phase, and ATP levels]; hydrogen peroxide (H2O2) production levels, mitochondrial aconitase activity, and malondialdehyde levels as well as non-enzymatic antioxidant defenses (vitamin E and glutathione levels) and enzymatic antioxidant defenses (glutathione disulfide reductase (GR), glutathione peroxidase (GPx), and manganese superoxide dismutase (MnSOD) activities). MG treatment induced a statistical significant decrease in RCR, aconitase and GR activities, and an increase in H2O2 production levels. The administration of PM did not counteract MG-induced effects and caused a significant decrease in ΔΨm. In mitochondria from control animals, PM caused an adaptive mechanism characterized by a decrease in aconitase and GR activities as well as an increase in both α-tocopherol levels and GPx and MnSOD activities. Altogether our results show that high levels of MG promote brain mitochondrial impairment and PM is not able to reverse MG-induced effects.