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      A gene to organism approach—assessing the impact of environmental pollution in eelpout ( Zoarces viviparus) females and larvae

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          Abstract

          A broad biomarker approach was applied to study the effects of marine pollution along the Swedish west coast using the teleost eelpout ( Zoarces viviparus) as the sentinel species. Measurements were performed on different biological levels, from the molecular to the organismal, including measurements of messenger RNA (mRNA), proteins, cellular and tissue changes, and reproductive success. Results revealed that eelpout captured in Stenungsund had significantly higher hepatic ethoxyresorufin O‐deethylase activity, high levels of both cytochrome P4501A and diablo homolog mRNA, and high prevalence of dead larvae and nuclear damage in erythrocytes. Eelpout collected in Göteborg harbor displayed extensive macrovesicular steatosis, whereby the majority of hepatocytes were affected throughout the liver, which could indicate an effect on lipid metabolism. Results also indicate that eelpouts collected at polluted sites might have an affected immune system, with lower mRNA expression of genes involved in the innate immune system and a higher number of lymphocytes. Biomarker assessment also was performed on livers dissected from unborn eelpout larvae collected from the ovary of the females. No significant differences were noted, which might indicate that the larvae to some extent are protected from effects of environmental pollutants. In conclusion, usage of the selected set of biological markers, covering responses from gene to organism, has demonstrated site‐specific biomarker patterns that provided a broad and comprehensive picture of the impact of environmental stressors. Environ Toxicol Chem 2015;34:1511–1523. © 2015 The Authors. Published by SETAC.

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          Environmentally induced oxidative stress in aquatic animals.

          Reactive oxygen species (ROS) are an unenviable part of aerobic life. Their steady-state concentration is a balance between production and elimination providing certain steady-state ROS level. The dynamic equilibrium can be disturbed leading to enhanced ROS level and damage to cellular constituents which is called "oxidative stress". This review describes the general processes responsible for ROS generation in aquatic animals and critically analyses used markers for identification of oxidative stress. Changes in temperature, oxygen levels and salinity can cause the stress in natural and artificial conditions via induction of disbalance between ROS production and elimination. Human borne pollutants can also enhance ROS level in hydrobionts. The role of transition metal ions, such as copper, chromium, mercury and arsenic, and pesticides, namely insecticides, herbicides, and fungicides along with oil products in induction of oxidative stress is highlighted. Last years the research in biology of free radicals was refocused from only descriptive works to molecular mechanisms with particular interest to ones enhancing tolerance. The function of some transcription regulators (Keap1-Nrf2 and HIF-1α) in coordination of organisms' response to oxidative stress is discussed. The future directions in the field are related with more accurate description of oxidative stress, the identification of its general characteristics and mechanisms responsible for adaptation to the stress have been also discussed. The last part marks some perspectives in the study of oxidative stress in hydrobionts, which, in addition to classic use, became more and more popular to address general biological questions such as development, aging and pathologies. Copyright © 2010 Elsevier B.V. All rights reserved.
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            Molecular biomarkers of oxidative stress in aquatic organisms in relation to toxic environmental pollutants.

            The potential of oxygen free radicals and other reactive oxygen species (ROS) to damage tissues and cellular components, called oxidative stress, in biological systems has become a topic of significant interest for environmental toxicology studies. The balance between prooxidant endogenous and exogenous factors (i.e., environmental pollutants) and antioxidant defenses (enzymatic and nonenzymatic) in biological systems can be used to assess toxic effects under stressful environmental conditions, especially oxidative damage induced by different classes of chemical pollutants. The role of these antioxidant systems and their sensitivity can be of great importance in environmental toxicology studies. In the past decade, numerous studies on the effects of oxidative stress caused by some environmental pollutants in terrestrial and aquatic species were published. Increased numbers of agricultural and industrial chemicals are entering the aquatic environment and being taken up into tissues of aquatic organisms. Transition metals, polycyclic aromatic hydrocarbons, organochlorine and organophosphate pesticides, polychlorinated biphenyls, dioxins, and other xenobiotics play important roles in the mechanistic aspects of oxidative damage. Such a diverse array of pollutants stimulate a variety of toxicity mechanisms, such as oxidative damage to membrane lipids, DNA, and proteins and changes to antioxidant enzymes. Although there are considerable gaps in our knowledge of cellular damage, response mechanisms, repair processes, and disease etiology in biological systems, free radical reactions and the production of toxic ROS are known to be responsible for a variety of oxidative damages leading to adverse health effects and diseases. In the past decade, mammalian species were used as models for the study of molecular biomarkers of oxidative stress caused by environmental pollutants to elucidate the mechanisms underlying cellular oxidative damage and to study the adverse effects of some environmental pollutants with oxidative potential in chronic exposure and/or sublethal concentrations. This review summarizes current knowledge and advances in the understanding of such oxidative processes in biological systems. This knowledge is extended to specific applications in aquatic organisms because of their sensitivity to oxidative pollutants, their filtration capacity, and their potential for environmental toxicology studies.
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              Identification of a novel hypoxia-inducible factor 1-responsive gene, RTP801, involved in apoptosis.

              Hypoxia is an important factor that elicits numerous physiological and pathological responses. One of the major gene expression programs triggered by hypoxia is mediated through hypoxia-responsive transcription factor hypoxia-inducible factor 1 (HIF-1). Here, we report the identification and cloning of a novel HIF-1-responsive gene, designated RTP801. Its strong up-regulation by hypoxia was detected both in vitro and in vivo in an animal model of ischemic stroke. When induced from a tetracycline-repressible promoter, RTP801 protected MCF7 and PC12 cells from hypoxia in glucose-free medium and from H(2)O(2)-triggered apoptosis via a dramatic reduction in the generation of reactive oxygen species. However, expression of RTP801 appeared toxic for nondividing neuron-like PC12 cells and increased their sensitivity to ischemic injury and oxidative stress. Liposomal delivery of RTP801 cDNA to mouse lungs also resulted in massive cell death. Thus, the biological effect of RTP801 overexpression depends on the cell context and may be either protecting or detrimental for cells under conditions of oxidative or ischemic stresses. Altogether, the data suggest a complex type of involvement of RTP801 in the pathogenesis of ischemic diseases.
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                Author and article information

                Journal
                Environ Toxicol Chem
                Environ. Toxicol. Chem
                10.1002/(ISSN)1552-8618
                ETC
                Environmental Toxicology and Chemistry / Setac
                John Wiley and Sons Inc. (Hoboken )
                0730-7268
                1552-8618
                July 2015
                18 June 2015
                : 34
                : 7 ( doiID: 10.1002/etc.v34.7 )
                : 1511-1523
                Affiliations
                [ 1 ] Department of Biological and Environmental SciencesUniversity of Gothenburg GothenburgSweden
                [ 2 ] Department of Clinic and Experimental MedicineUniversity of Pisa PisaItaly
                [ 3 ] Centre for EnvironmentFisheries and Aquaculture Science Weymouth DorsetUnited Kingdom
                [ 4 ] Department of Aquatic Resources, Institute of Coastal ResearchSwedish University of Agricultural Sciences VäröbackaSweden
                [ 5 ] Department of Mathematical StatisticsChalmers University of Technology GothenburgSweden
                Author notes
                [*] [* ]Address correspondence to noomi.asker@ 123456bioenv.gu.se
                Article
                ETC2921
                10.1002/etc.2921
                5008212
                25663503
                0789bab4-bb5a-47fd-87b4-30d4ca39307a
                © 2015 The Authors. Published by SETAC.

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 17 September 2014
                : 26 October 2014
                : 01 February 2015
                Page count
                Pages: 13
                Funding
                Funded by: Swedish Environmental Protection Agency, the Science Faculty strategic research platform “Ecotoxicology—From Gene to Ocean”
                Categories
                Environmental Toxicology
                Environmental Toxicology
                Custom metadata
                2.0
                etc2921
                July 2015
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:01.09.2016

                Environmental chemistry
                biomarker,histopathology,genotoxicity,gene expression,eelpout
                Environmental chemistry
                biomarker, histopathology, genotoxicity, gene expression, eelpout

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