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      Oxidative Stress and Its Significant Roles in Neurodegenerative Diseases and Cancer

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          Abstract

          Reactive oxygen and nitrogen species have been implicated in diverse pathophysiological conditions, including inflammation, neurodegenerative diseases and cancer. Accumulating evidence indicates that oxidative damage to biomolecules including lipids, proteins and DNA, contributes to these diseases. Previous studies suggest roles of lipid peroxidation and oxysterols in the development of neurodegenerative diseases and inflammation-related cancer. Our recent studies identifying and characterizing carbonylated proteins reveal oxidative damage to heat shock proteins in neurodegenerative disease models and inflammation-related cancer, suggesting dysfunction in their antioxidative properties. In neurodegenerative diseases, DNA damage may not only play a role in the induction of apoptosis, but also may inhibit cellular division via telomere shortening. Immunohistochemical analyses showed co-localization of oxidative/nitrative DNA lesions and stemness markers in the cells of inflammation-related cancers. Here, we review oxidative stress and its significant roles in neurodegenerative diseases and cancer.

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          Most cited references124

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          Determination of carbonyl content in oxidatively modified proteins.

          R L Levine, D Garland, C. Oliver … (1990)
          Article 0 comments Cited 439 times – based on 0 reviews     Review now
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            Exome sequencing identifies distinct mutational patterns in liver fluke-related and non-infection-related bile duct cancers.

            Waraporn Chan-On, Maarja-Liisa Nairismägi, Choon Kiat Ong … (2013)
            The impact of different carcinogenic exposures on the specific patterns of somatic mutation in human tumors remains unclear. To address this issue, we profiled 209 cholangiocarcinomas (CCAs) from Asia and Europe, including 108 cases caused by infection with the liver fluke Opisthorchis viverrini and 101 cases caused by non-O. viverrini-related etiologies. Whole-exome sequencing (n = 15) and prevalence screening (n = 194) identified recurrent somatic mutations in BAP1 and ARID1A, neither of which, to our knowledge, has previously been reported to be mutated in CCA. Comparisons between intrahepatic O. viverrini-related and non-O. viverrini-related CCAs demonstrated statistically significant differences in mutation patterns: BAP1, IDH1 and IDH2 were more frequently mutated in non-O. viverrini CCAs, whereas TP53 mutations showed the reciprocal pattern. Functional studies demonstrated tumor suppressive functions for BAP1 and ARID1A, establishing the role of chromatin modulators in CCA pathogenesis. These findings indicate that different causative etiologies may induce distinct somatic alterations, even within the same tumor type.
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              Role of oxidative carbonylation in protein quality control and senescence.

              Thomas Nyström (2005)
              Proteins can become modified by a large number of reactions involving reactive oxygen species. Among these reactions, carbonylation has attracted a great deal of attention due to its irreversible and unrepairable nature. Carbonylated proteins are marked for proteolysis by the proteasome and the Lon protease but can escape degradation and form high-molecular-weight aggregates that accumulate with age. Such carbonylated aggregates can become cytotoxic and have been associated with a large number of age-related disorders, including Parkinson's disease, Alzheimer's disease, and cancer. This review focuses on the generation of and defence against protein carbonyls and speculates on the potential role of carbonylation in protein quality control, cellular deterioration, and senescence.
              Article 0 comments Cited 178 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Guillermo T. Sáez: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 24 December 2014
                Publication date Collection: January 2015
                Volume: 16
                Issue: 1
                Pages: 193-217
                Affiliations
                [1 ]Department of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand; E-Mails: rothanan@ 123456yahoo.com (R.T.); puangrat@ 123456kku.ac.th (P.Y.)
                [2 ]Liver Fluke and Cholangiocarcinoma Research Center, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand; E-Mail: mrsomchaip@ 123456yahoo.com
                [3 ]Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan; E-Mails: s-oikawa@ 123456doc.medic.mie-u.ac.jp (S.O.); y-hiraku@ 123456doc.medic.mie-u.ac.jp (Y.H.)
                [4 ]Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Suzuka, Mie 513-8670, Japan; E-Mails: shiho-o@ 123456suzuka-u.ac.jp (S.O.); kawanisi@ 123456suzuka-u.ac.jp (S.K.)
                [5 ]Faculty of Nursing Science, Suzuka University of Medical Science, Suzuka, Mie 513-8670, Japan; E-Mail: maning@ 123456suzuka-u.ac.jp
                [6 ]Department of Parasitology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: mmurata@ 123456doc.medic.mie-u.ac.jp ; Tel./Fax: +81-59-231-5011.
                Article
                Publisher ID: ijms-16-00193
                DOI: 10.3390/ijms16010193
                PMC ID: 4307243
                PubMed ID: 25547488
                SO-VID: edb3b83c-7e8f-46b3-9412-de97e05798f1
                Copyright © © 2014 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 04 October 2014
                Date accepted : 05 December 2014
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: oxidative stress,neurodegenerative diseases,cancer,lipid peroxidation,oxysterol,carbonyl proteins,protein damage,dna damage,stem cells
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: oxidative stress, neurodegenerative diseases, cancer, lipid peroxidation, oxysterol, carbonyl proteins, protein damage, dna damage, stem cells

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