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      Predictive and Prognostic Biomarkers of Respiratory Diseases due to Particulate Matter Exposure

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          Abstract

          Air pollution is getting severe and concerns about its toxicity effects on airway and lung disease are also increasing. Particulate matter (PM) is major component of air pollutant. It causes respiratory diseases, such as asthma, chronic obstructive pulmonary disease, lung cancer, and so on. PM particles enter the airway and lung by inhalation, causing damages to them. Especially, PM 2.5 can penetrate into the alveolus and pass to the systemic circulation. It can affect the cardiopulmonary system and cause cardiopulmonary disorders. In this review, we focused on PM-inducing toxicity mechanisms in the framework of oxidative stress, inflammation, and epigenetic changes. We also reviewed its correlation with respiratory diseases. In addition, we reviewed biomarkers related to PM-induced respiratory diseases. These biomarkers might be used for disease prediction and early diagnosis. With recent trend of using genomic analysis tools in the field of toxicogenomics, respiratory disease biomarkers associated with PM will be continuously investigated. Effective biomarkers derived from earlier studies and further studies might be utilized to reduce respiratory diseases.

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          Reactive oxygen species promote TNFalpha-induced death and sustained JNK activation by inhibiting MAP kinase phosphatases.

          TNFalpha is a pleiotropic cytokine that induces either cell proliferation or cell death. Inhibition of NF-kappaB activation increases susceptibility to TNFalpha-induced death, concurrent with sustained JNK activation, an important contributor to the death response. Sustained JNK activation in NF-kappaB-deficient cells was suggested to depend on reactive oxygen species (ROS), but how ROS affect JNK activation was unclear. We now show that TNFalpha-induced ROS, whose accumulation is suppressed by mitochondrial superoxide dismutase, cause oxidation and inhibition of JNK-inactivating phosphatases by converting their catalytic cysteine to sulfenic acid. This results in sustained JNK activation, which is required for cytochrome c release and caspase 3 cleavage, as well as necrotic cell death. Treatment of cells or experimental animals with an antioxidant prevents H(2)O(2) accumulation, JNK phosphatase oxidation, sustained JNK activity, and both forms of cell death. Antioxidant treatment also prevents TNFalpha-mediated fulminant liver failure without affecting liver regeneration.
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            Free Radicals in Biology and Medicine

            Free Radicals in Biology and Medicine has become a classic text in the field of free radical and antioxidant research since its first publication in 1985. <br> This latest edition has been comprehensively rewritten and updated (over 80% of the text is new), while maintaining the clarity of its predecessor. There is expanded coverage of isoprostanes and related compounds, mechanisms of oxidative damage to DNA and proteins (and the repair of such damage), the free radical theory of aging and the roles played by reactive species in signal transduction, cell death, human reproduction, and other important biological events. Greater emphasis has also been placed on the methods available to measure reactive species and oxidative damage (and their potential pitfalls), as well as the importance of antioxidants in the human diet. <br> This book is recommended as a comprehensive introduction to the field for students, clinicians and researchers, and an invaluable companion to all those interested in the role of free radicals in the life and biomedical sciences.
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              Free radicals in biology and medicine

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                Author and article information

                Journal
                J Cancer Prev
                J Cancer Prev
                JCP
                Journal of Cancer Prevention
                Korean Society of Cancer Prevention
                2288-3649
                2288-3657
                March 2017
                30 March 2017
                : 22
                : 1
                : 6-15
                Affiliations
                [1 ]Institute of Environmental Medicine for Green Chemistry, Department of Life Science, Dongguk Bio-Med Campus, Dongguk University, Goyang, Korea
                [2 ]Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University College of Medicine, Seoul, Korea
                Author notes
                Correspondence to: Young Rok Seo, Institute of Environmental Medicine for Green Chemistry, Department of Life Science, Dongguk Bio-Med Campus, Dongguk University, 32 Dongguk-ro, Ilsandong-gu, Goyang 10326, Korea, Tel: +82-31-961-5172, E-mail: seoyr@ 123456dongguk.edu
                Article
                jcp-22-006
                10.15430/JCP.2017.22.1.6
                5380184
                28382281
                ce18e08a-1206-4474-b934-244bcdaa5cef
                Copyright © 2017 Korean Society of Cancer Prevention

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 21 December 2016
                : 09 February 2017
                : 10 February 2017
                Categories
                Review

                particulate matter,biomarker,oxidative stress,inflammation,epigenetic change

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