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      The Molecular Mechanisms of Adaptive Response Related to Environmental Stress

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          Abstract

          The exposure of living organisms to environmental stress triggers defensive responses resulting in the activation of protective processes. Whenever the exposure occurs at low doses, defensive effects overwhelm the adverse effects of the exposure; this adaptive situation is referred to as “hormesis”. Environmental, physical, and nutritional hormetins lead to the stimulation and strengthening of the maintenance and repair systems in cells and tissues. Exercise, heat, and irradiation are examples of physical hormetins, which activate heat shock-, DNA repair-, and anti-oxidative-stress responses. The health promoting effect of many bio-actives in fruits and vegetables can be seen as the effect of mildly toxic compounds triggering this adaptive stimulus. Numerous studies indicate that living organisms possess the ability to adapt to adverse environmental conditions, as exemplified by the fact that DNA damage and gene expression profiling in populations living in the environment with high levels of air pollution do not correspond to the concentrations of pollutants. The molecular mechanisms of the hormetic response include modulation of (a) transcription factor Nrf2 activating the synthesis of glutathione and the subsequent protection of the cell; (b) DNA methylation; and (c) microRNA. These findings provide evidence that hormesis is a toxicological event, occurring at low exposure doses to environmental stressors, having the benefit for the maintenance of a healthy status.

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          Most cited references86

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          Cancer chemoprevention with dietary phytochemicals.

          Chemoprevention refers to the use of agents to inhibit, reverse or retard tumorigenesis. Numerous phytochemicals derived from edible plants have been reported to interfere with a specific stage of the carcinogenic process. Many mechanisms have been shown to account for the anticarcinogenic actions of dietary constituents, but attention has recently been focused on intracellular-signalling cascades as common molecular targets for various chemopreventive phytochemicals.
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            DNA methylation patterns and epigenetic memory.

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              Persistent epigenetic differences associated with prenatal exposure to famine in humans.

              Extensive epidemiologic studies have suggested that adult disease risk is associated with adverse environmental conditions early in development. Although the mechanisms behind these relationships are unclear, an involvement of epigenetic dysregulation has been hypothesized. Here we show that individuals who were prenatally exposed to famine during the Dutch Hunger Winter in 1944-45 had, 6 decades later, less DNA methylation of the imprinted IGF2 gene compared with their unexposed, same-sex siblings. The association was specific for periconceptional exposure, reinforcing that very early mammalian development is a crucial period for establishing and maintaining epigenetic marks. These data are the first to contribute empirical support for the hypothesis that early-life environmental conditions can cause epigenetic changes in humans that persist throughout life.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                25 September 2020
                October 2020
                : 21
                : 19
                : 7053
                Affiliations
                [1 ]Department of Genetic Toxicology and Epigenetics, Institute of Experimental Medicine, 14220 Prague, Czech Republic; andrea.rossnerova@ 123456iem.cas.cz
                [2 ]Department of Experimental Medicine, University of Genoa, 16132 Genoa, Italy; izzotti@ 123456unige.it
                [3 ]IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy
                [4 ]Department of Health Science, University of Genoa, 16132 Genoa, Italy
                [5 ]Department of Pharmacology and Toxicology, Maastricht University, 6200 MD Maastricht, The Netherlands; a.bast@ 123456maastrichtuniversity.nl
                [6 ]Campus Venlo, Maastricht University, 5900 AA Venlo, The Netherlands
                [7 ]Department of Molecular Biology and Genetics, Aarhus University, 8000 Aarhus, Denmark; rattan@ 123456mbg.au.dk
                [8 ]Department of Nanotoxicology and Molecular Epidemiology, Institute of Experimental Medicine, 14220 Prague, Czech Republic; prossner@ 123456biomed.cas.cz
                Author notes
                Author information
                https://orcid.org/0000-0002-5383-2789
                Article
                ijms-21-07053
                10.3390/ijms21197053
                7582272
                32992730
                901cb724-583b-459a-811c-283cfffe2061
                © 2020 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 (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 10 August 2020
                : 22 September 2020
                Categories
                Review

                Molecular biology
                adaptive response,preventive medicine,microrna machinery
                Molecular biology
                adaptive response, preventive medicine, microrna machinery

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