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      Redox toxicology of environmental chemicals causing oxidative stress

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          Abstract

          Living organisms are surrounded with heavy metals such as methylmercury, manganese, cobalt, cadmium, arsenic, as well as pesticides such as deltamethrin and paraquat, or atmospheric pollutants such as quinone. Extensive studies have demonstrated a strong link between environmental pollutants and human health. Redox toxicity is proposed as one of the main mechanisms of chemical-induced pathology in humans. Acting as both a sensor of oxidative stress and a positive regulator of antioxidants, the nuclear factor erythroid 2-related factor 2 (NRF2) has attracted recent attention. However, the role NRF2 plays in environmental pollutant-induced toxicity has not been systematically addressed. Here, we characterize NRF2 function in response to various pollutants, such as metals, pesticides and atmospheric quinones. NRF2 related signaling pathways and epigenetic regulations are also reviewed.

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          Highlights

          • •

            Environmental chemicals cause redox toxicity via oxidative stress.

          • •

            NRF2 acts as a sensor of oxidative stress and a positive regulator of antioxidants.

          • •

            NRF2 responds to metals, pesticides and atmospheric pollutants.

          • •

            NRF2 and related pathways can be epigenetically regulated.

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          A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

          Stephen S Lim, Theo Vos, Abraham D. Flaxman … (2012)
          The Lancet, 380(9859), 2224-2260
          Article 0 comments Cited 3806 times – based on 0 reviews     Review now
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            NRF2 and the Hallmarks of Cancer

            Donna Zhang, Montserrat Rojo de la Vega, Eli Chapman (2018)
            The transcription factor NRF2 is the master regulator of the cellular antioxidant response. Though recognized originally as a target of chemopreventive compounds that help prevent cancer and other maladies, accumulating evidence has established the NRF2 pathway as a driver of cancer progression, metastasis, and resistance to therapy. Recent studies have identified new functions for NRF2 in the regulation of metabolism and other essential cellular functions, establishing NRF2 as a truly pleiotropic transcription factor. In this review, we explore the roles of NRF2 in the hallmarks of cancer, indicating both tumor suppressive and tumor-promoting effects.
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              Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution.

              C. Arden Pope III (2002)
              Associations have been found between day-to-day particulate air pollution and increased risk of various adverse health outcomes, including cardiopulmonary mortality. However, studies of health effects of long-term particulate air pollution have been less conclusive. To assess the relationship between long-term exposure to fine particulate air pollution and all-cause, lung cancer, and cardiopulmonary mortality. Vital status and cause of death data were collected by the American Cancer Society as part of the Cancer Prevention II study, an ongoing prospective mortality study, which enrolled approximately 1.2 million adults in 1982. Participants completed a questionnaire detailing individual risk factor data (age, sex, race, weight, height, smoking history, education, marital status, diet, alcohol consumption, and occupational exposures). The risk factor data for approximately 500 000 adults were linked with air pollution data for metropolitan areas throughout the United States and combined with vital status and cause of death data through December 31, 1998. All-cause, lung cancer, and cardiopulmonary mortality. Fine particulate and sulfur oxide--related pollution were associated with all-cause, lung cancer, and cardiopulmonary mortality. Each 10-microg/m(3) elevation in fine particulate air pollution was associated with approximately a 4%, 6%, and 8% increased risk of all-cause, cardiopulmonary, and lung cancer mortality, respectively. Measures of coarse particle fraction and total suspended particles were not consistently associated with mortality. Long-term exposure to combustion-related fine particulate air pollution is an important environmental risk factor for cardiopulmonary and lung cancer mortality.
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                Author and article information

                Contributors
                Fuli Zheng
                Huangyuan Li
                Yoshito Kumagai
                Michael Aschner
                Journal
                Journal ID (nlm-ta): Redox Biol
                Journal ID (iso-abbrev): Redox Biol
                Title: Redox Biology
                Publisher: Elsevier
                ISSN (Electronic): 2213-2317
                Publication date PMC-release: 18 April 2020
                Publication date Collection: July 2020
                Publication date (Electronic): 18 April 2020
                Volume: 34
                Electronic Location Identifier: 101475
                Affiliations
                [a ]Department of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou, Fujian, 350122, China
                [b ]Department of Molecular Pharmacology, Albert Einstein College of Medicine, Forchheimer 209, 1300 Morris Park Avenue, Bronx, NY, 10461, United States
                [c ]Environmental Biology Laboratory, Faculty of Medicine, University of Tsukuba, Tsukuba, 305-8575, Japan
                Author notes
                [∗ ]Corresponding author. Department of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou, Fujian, 350122, China. f.zheng@ 123456fjmu.edu.cn
                [∗∗ ]Corresponding author. lhy@ 123456fjmu.edu.cn
                [∗∗∗ ]Corresponding author. yk-em-tu@ 123456md.tsukuba.ac.jp
                [∗∗∗∗ ]Corresponding author. michael.aschner@ 123456einsteinmed.org
                Article
                Publisher ID: S2213-2317(19)31511-3 Publisher ID: 101475
                DOI: 10.1016/j.redox.2020.101475
                PMC ID: 7327986
                PubMed ID: 32336668
                SO-VID: cff133bb-a7d8-4bf9-8da1-853e6b75e056
                Copyright © © 2020 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 4 December 2019
                Date revision received : 18 February 2020
                Date accepted : 20 February 2020
                Categories
                Subject: Articles from the Special Issue on Impact of environmental pollution and stress on redox signaling and oxidative stress pathways; Edited by Thomas Münzel and Andreas Daiber

                Keywords: nrf2,heavy metals,pesticides,air pollutants,epigenetic modifications,redox signaling pathways
                Data availability:
                Keywords: nrf2, heavy metals, pesticides, air pollutants, epigenetic modifications, redox signaling pathways

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