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      Magnesium deficiency and oxidative stress: an update

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          Abstract

          Magnesium deficiency (MgD) has been shown to impact numerous biological processes at the cellular and molecular levels. In the present review, we discuss the relationship between MgD and oxidative stress (OS). MgD is accompanied by increased levels of OS markers such as lipid, protein and DNA oxidative modification products. Additionally, a relationship was detected between MgD and a weakened antioxidant defence. Different mechanisms associated with MgD are involved in the development and maintenance of OS. These mechanisms include systemic reactions such as inflammation and endothelial dysfunction, as well as changes at the cellular level, such as mitochondrial dysfunction and excessive fatty acid production.

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          Lipid peroxidation and antioxidants as biomarkers of tissue damage.

          J Gutteridge (1995)
          Disturbance of the balance between the production of reactive oxygen species such as superoxide; hydrogen peroxide; hypochlorous acid; hydroxyl, alkoxyl, and peroxyl radicals; and antioxidant defenses against them produces oxidative stress, which amplifies tissue damage by releasing prooxidative forms of reactive iron that are able to drive Fenton chemistry and lipid peroxidation and by eroding away protective sacrificial antioxidants. The body has a hierarchy of defense strategies to deal with oxidative stress within different cellular compartments, and superimposed on these are gene-regulated defenses involving the heat-shock and oxidant stress proteins.
          Article 0 comments Cited 239 times – based on 0 reviews     Review now
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            Lipid hydroperoxide generation, turnover, and effector action in biological systems.

            Luis A Girotti (1998)
            Lipid peroxidation is a well known example of oxidative damage in cell membranes, lipoproteins, and other lipid-containing structures. Peroxidative modification of unsaturated phospholipids, glycolipids, and cholesterol can occur in reactions triggered by i) free radical species such as oxyl radicals, peroxyl radicals, and hydroxyl radicals derived from iron-mediated reduction of hydrogen peroxide or ii) non-radical species such as singlet oxygen, ozone, and peroxynitrite generated by the reaction of superoxide with nitric oxide. Lipid hydroperoxides (LOOHs) are prominent non-radical intermediates of lipid peroxidation whose identification can often provide valuable mechanistic information, e.g., whether a primary reaction is mediated by singlet oxygen or oxyradicals. Certain cholesterol-derived hydroperoxides (ChOOHs) have been used very effectively in this regard, both in model systems and cells. Being more polar than parent lipids, LOOHs perturb membrane structure/function and can be deleterious to cells on this basis alone. However, LOOHs can also participate in redox reactions, the nature and magnitude of which often determines whether peroxidative injury is exacerbated or prevented. Exacerbation may reflect iron-catalyzed one-electron reduction of LOOHs, resulting in free radical-mediated chain peroxidation, whereas prevention may reflect selenoperoxidase-catalyzed two-electron reduction of LOOHs to relatively non-toxic alcohols. LOOH partitioning between these two pathways in an oxidatively stressed cell is still poorly understood, but recent cell studies involving various ChOOHs have begun to shed light on this important question. An aspect of related interest that is under intensive investigation is lipid peroxidation/LOOH-mediated stress signaling, which may evoke a variety of cellular responses, ranging from induction of antioxidant enzymes to apoptotic death. Ongoing exploration of these processes will have important bearing on our understanding of disease states associated with peroxidative stress.
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              Magnesium metabolism and its disorders.

              R. Swaminathan (2003)
              Magnesium is the fourth most abundant cation in the body and plays an important physiological role in many of its functions. Magnesium balance is maintained by renal regulation of magnesium reabsorption. The exact mechanism of the renal regulation is not fully understood. Magnesium deficiency is a common problem in hospital patients, with a prevalence of about 10%. There are no readily available and easy methods to assess magnesium status. Serum magnesium and the magnesium tolerance test are the most widely used. Measurement of ionised magnesium may become more widely available with the availability of ion selective electrodes. Magnesium deficiency and hypomagnesaemia can result from a variety of causes including gastrointestinal and renal losses. Magnesium deficiency can cause a wide variety of features including hypocalcaemia, hypokalaemia and cardiac and neurological manifestations. Chronic low magnesium state has been associated with a number of chronic diseases including diabetes, hypertension, coronary heart disease, and osteoporosis. The use of magnesium as a therapeutic agent in asthma, myocardial infarction, and pre-eclampsia is also discussed. Hypermagnesaemia is less frequent than hypomagnesaemia and results from failure of excretion or increased intake. Hypermagnesaemia can lead to hypotension and other cardiovascular effects as well as neuromuscular manifestations. Causes and management of hypermagnesaemia are discussed.
              Article 0 comments Cited 143 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Igor N. Iezhitsa: iezhitsa@salam.uitm.edu.my , iezhitsa@yandex.ru
                Journal
                Journal ID (nlm-ta): Biomedicine (Taipei)
                Journal ID (iso-abbrev): Biomedicine (Taipei)
                Title: BioMedicine
                Publisher: China Medical University (Taichung )
                ISSN (Print): 2211-8020
                ISSN (Electronic): 2211-8039
                Publication date (Electronic): 17 November 2016
                Publication date PMC-release: 17 November 2016
                Publication date Collection: December 2016
                Volume: 6
                Issue: 4
                Electronic Location Identifier: 20
                Affiliations
                [1 ]Department of Pharmacology, Volgograd State Medical University, Pl. Pavshikh Bortsov, 1, Volgograd, 400131 Russia
                [2 ]Department of Immunology and Allergology, Volgograd State Medical University, Pl. Pavshikh Bortsov, 1, Volgograd, 400131 Russia
                [3 ]Institute of Pharmacy, Department of Pharmacology and Toxicology, University of Innsbruck, Center for Chemistry and Biomedicine, Innrain 80-82/III, A-6020, Innsbruck, Austria
                [4 ]Centre for Neuroscience Research (NeuRon), Faculty of Medicine, Universiti Teknologi MARA (UiTM), Sungai Buloh Campus, Jalan Hospital, 47000 Sungai Buloh, Selangor Darul Ehsan Malaysia
                [5 ]RIG “Molecular Pharmacology and Advanced Therapeutics”, Pharmaceutical & Life Sciences (PLS) Communities of Research (CoRe),, Universiti Teknologi MARA, 40450 Shah Alam, Selangor Darul Ehsan Malaysia
                [6 ]Faculty of Medicine, Sungai Buloh Campus, Jalan Hospital, Universiti Teknologi MARA, 47000 Sungai Buloh, Selangor Darul Ehsan Malaysia
                Article
                Publisher ID: 20
                DOI: 10.7603/s40681-016-0020-6
                PMC ID: 5112180
                PubMed ID: 27854048
                SO-VID: ecac7f9e-0a07-453c-ba1f-87bfbcb5e40d
                Copyright © © China Medical University 2016
                History
                Date received : 19 May 2016
                Date accepted : 23 September 2016
                Categories
                Subject: Review Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2016

                Keywords: magnesium,magnesium deficiency,oxidative stress,antioxidants,reactive oxygen species,lipid peroxidation
                Data availability:
                Keywords: magnesium, magnesium deficiency, oxidative stress, antioxidants, reactive oxygen species, lipid peroxidation

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