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      Monosodium glutamate-induced oxidative kidney damage and possible mechanisms: a mini-review

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          Abstract

          Animal studies suggest that chronic monosodium glutamate (MSG) intake induces kidney damage by oxidative stress. However, the underlying mechanisms are still unclear, despite the growing evidence and consensus that α-ketoglutarate dehydrogenase, glutamate receptors and cystine-glutamate antiporter play an important role in up-regulation of oxidative stress in MSG-induced renal toxicity. This review summaries evidence from studies into MSG-induced renal oxidative damage, possible mechanisms and their importance from a toxicological viewpoint.

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          The free radical theory of aging matures.

          K Beckman, B N AMES (1998)
          The free radical theory of aging, conceived in 1956, has turned 40 and is rapidly attracting the interest of the mainstream of biological research. From its origins in radiation biology, through a decade or so of dormancy and two decades of steady phenomenological research, it has attracted an increasing number of scientists from an expanding circle of fields. During the past decade, several lines of evidence have convinced a number of scientists that oxidants play an important role in aging. (For the sake of simplicity, we use the term oxidant to refer to all "reactive oxygen species," including O2-., H2O2, and .OH, even though the former often acts as a reductant and produces oxidants indirectly.) The pace and scope of research in the last few years have been particularly impressive and diverse. The only disadvantage of the current intellectual ferment is the difficulty in digesting the literature. Therefore, we have systematically reviewed the status of the free radical theory, by categorizing the literature in terms of the various types of experiments that have been performed. These include phenomenological measurements of age-associated oxidative stress, interspecies comparisons, dietary restriction, the manipulation of metabolic activity and oxygen tension, treatment with dietary and pharmacological antioxidants, in vitro senescence, classical and population genetics, molecular genetics, transgenic organisms, the study of human diseases of aging, epidemiological studies, and the ongoing elucidation of the role of active oxygen in biology.
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            Normal oxidative damage to mitochondrial and nuclear DNA is extensive.

            C. Richter, J Park, B N AMES (1988)
            Oxidative damage to DNA can be caused by excited oxygen species, which are produced by radiation or are by-products of aerobic metabolism. The oxidized base, 8-hydroxydeoxyguanosine (oh8dG), 1 of approximately 20 known radiation damage products, has been assayed in the DNA of rat liver. oh8dG is present at a level of 1 per 130,000 bases in nuclear DNA and 1 per 8000 bases in mtDNA. Mitochondria treated with various prooxidants have an increased level of oh8dG. The high level of oh8dG in mtDNA may be caused by the immense oxygen metabolism, relatively inefficient DNA repair, and the absence of histones in mitochondria. It may be responsible for the observed high mutation rate of mtDNA.
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              Requirement for generation of H2O2 for platelet-derived growth factor signal transduction.

              M Sundaresan, Z X Yu, V Ferrans … (1995)
              Stimulation of rat vascular smooth muscle cells (VSMCs) by platelet-derived growth factor (PDGF) transiently increased the intracellular concentration of hydrogen peroxide (H2O2). This increase could be blunted by increasing the intracellular concentration of the scavenging enzyme catalase or by the chemical antioxidant N-acetylcysteine. The response of VSMCs to PDGF, which includes tyrosine phosphorylation, mitogen-activated protein kinase stimulation, DNA synthesis, and chemotaxis, was inhibited when the growth factor-stimulated rise in H2O2 concentration was blocked. These results suggest that H2O2 may act as a signal-transducing molecule, and they suggest a potential mechanism for the cardioprotective effects of antioxidants.
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                Author and article information

                Contributors
                Amod Sharma: amod.sha@mahidol.ac.th
                Journal
                Journal ID (nlm-ta): J Biomed Sci
                Journal ID (iso-abbrev): J. Biomed. Sci
                Title: Journal of Biomedical Science
                Publisher: BioMed Central (London )
                ISSN (Print): 1021-7770
                ISSN (Electronic): 1423-0127
                Publication date (Electronic): 22 October 2015
                Publication date PMC-release: 22 October 2015
                Publication date Collection: 2015
                Volume: 22
                Electronic Location Identifier: 93
                Affiliations
                [ ]Department of Physiology, Siriraj Hospital, Mahidol University, Bangkok, 10700 Thailand
                [ ]Department of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002 Thailand
                Article
                Publisher ID: 192
                DOI: 10.1186/s12929-015-0192-5
                PMC ID: 4618747
                PubMed ID: 26493866
                SO-VID: 7832cdbe-2f9b-4b9c-bacc-bcd67ab5908f
                Copyright © © Sharma. 2015
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 24 August 2015
                Date accepted : 6 October 2015
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2015

                ScienceOpen disciplines: Molecular medicine
                Keywords: monosodium glutamate,kidney,oxidative stress,glutamate receptors,α-ketoglutarate dehydrogenase
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: monosodium glutamate, kidney, oxidative stress, glutamate receptors, α-ketoglutarate dehydrogenase

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