73
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Manganese Superoxide Dismutase: Guardian of the Powerhouse

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The mitochondrion is vital for many metabolic pathways in the cell, contributing all or important constituent enzymes for diverse functions such as β-oxidation of fatty acids, the urea cycle, the citric acid cycle, and ATP synthesis. The mitochondrion is also a major site of reactive oxygen species (ROS) production in the cell. Aberrant production of mitochondrial ROS can have dramatic effects on cellular function, in part, due to oxidative modification of key metabolic proteins localized in the mitochondrion. The cell is equipped with myriad antioxidant enzyme systems to combat deleterious ROS production in mitochondria, with the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) acting as the chief ROS scavenging enzyme in the cell. Factors that affect the expression and/or the activity of MnSOD, resulting in diminished antioxidant capacity of the cell, can have extraordinary consequences on the overall health of the cell by altering mitochondrial metabolic function, leading to the development and progression of numerous diseases. A better understanding of the mechanisms by which MnSOD protects cells from the harmful effects of overproduction of ROS, in particular, the effects of ROS on mitochondrial metabolic enzymes, may contribute to the development of novel treatments for various diseases in which ROS are an important component.

          Related collections

          Most cited references355

          • Record: found
          • Abstract: not found
          • Article: not found

          On the origin of cancer cells.

          O WARBURG (1956)
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Mitochondria and apoptosis.

            D Green, J Reed (1998)
            A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins. The different signals that converge on mitochondria to trigger or inhibit these events and their downstream effects delineate several major pathways in physiological cell death.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The inflammasomes: guardians of the body.

              The innate immune system relies on its capacity to rapidly detect invading pathogenic microbes as foreign and to eliminate them. The discovery of Toll-like receptors (TLRs) provided a class of membrane receptors that sense extracellular microbes and trigger antipathogen signaling cascades. More recently, intracellular microbial sensors have been identified, including NOD-like receptors (NLRs). Some of the NLRs also sense nonmicrobial danger signals and form large cytoplasmic complexes called inflammasomes that link the sensing of microbial products and metabolic stress to the proteolytic activation of the proinflammatory cytokines IL-1beta and IL-18. The NALP3 inflammasome has been associated with several autoinflammatory conditions including gout. Likewise, the NALP3 inflammasome is a crucial element in the adjuvant effect of aluminum and can direct a humoral adaptive immune response. In this review, we discuss the role of NLRs, and in particular the inflammasomes, in the recognition of microbial and danger components and the role they play in health and disease.
                Bookmark

                Author and article information

                Journal
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                Molecular Diversity Preservation International (MDPI)
                1422-0067
                2011
                21 October 2011
                : 12
                : 10
                : 7114-7162
                Affiliations
                Graduate Center for Toxicology, University of Kentucky, 454 HSRB, 1095 VA Drive, Lexington, KY 40536, USA; E-Mails: aaron.holley@ 123456uky.edu (A.K.H.); vbakt2@ 123456uky.edu (V.B.); joycemarievr@ 123456hotmail.com (J.M.V.-R.)
                Author notes
                [* ] Author to whom correspondence should be addressed; E-Mail: dstcl00@ 123456uky.edu ; Tel.: +1-859-257-3956; Fax: +1-859-323-1059.
                Article
                ijms-12-07114
                10.3390/ijms12107114
                3211030
                22072939
                ad24bf18-3a25-4f2a-a02b-7ed13567a4bb
                © 2011 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                : 08 August 2011
                : 28 September 2011
                : 08 October 2011
                Categories
                Review

                Molecular biology
                manganese superoxide dismutase,cardiovascular disease,metabolism,cancer,oxidative stress,reactive oxygen species,mitochondria,neurodegenerative disorders

                Comments

                Comment on this article