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      Sub-lethal Doses of Polybrominated Diphenyl Ethers, in Vitro, Promote Oxidative Stress and Modulate Molecular Markers Related to Cell Cycle, Antioxidant Balance and Cellular Energy Management

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          Abstract

          In the present study, we evaluated the effects of different concentrations of the polybrominated diphenyl ethers (PBDEs) BDE-209, BDE-47 and BDE-99, on the vitality and oxidative stress of a HS-68 human cell culture exposed to the compounds for three days. The results showed that for this exposure time, only the highest concentrations produced a significant vitality reduction and oxidative stress induction ( p < 0.05), measured as reactive oxygen species (ROS). Subsequently, in order to verify the effects of sub-lethal doses, cells were exposed for a longer time and data collected, after 12 and 20 days, to study ROS production and some molecular markers related to cell cycle and stress (p53, pRB, PARP, c-Jun and c-Fos), antioxidant status and proliferation (ERK, c-Jun and c-Fos), energy balance (NRF2, AMPK, HIF). Most of the biomarkers were influenced by the treatments, indicating that sub-lethal doses of PBDEs, for longer time, can enhance the production of ROS, altering the energetic metabolism, cell cycle and antioxidant balance, determining possible negative effects on the cell proliferation equilibrium.

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          The first 30 years of p53: growing ever more complex.

          Thirty years ago p53 was discovered as a cellular partner of simian virus 40 large T-antigen, the oncoprotein of this tumour virus. The first decade of p53 research saw the cloning of p53 DNA and the realization that p53 is not an oncogene but a tumour suppressor that is very frequently mutated in human cancer. In the second decade of research, the function of p53 was uncovered: it is a transcription factor induced by stress, which can promote cell cycle arrest, apoptosis and senescence. In the third decade after its discovery new functions of this protein were revealed, including the regulation of metabolic pathways and cytokines that are required for embryo implantation. The fourth decade of research may see new p53-based drugs to treat cancer. What is next is anybody's guess.
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            Requirement for p53 and p21 to sustain G2 arrest after DNA damage.

            After DNA damage, many cells appear to enter a sustained arrest in the G2 phase of the cell cycle. It is shown here that this arrest could be sustained only when p53 was present in the cell and capable of transcriptionally activating the cyclin-dependent kinase inhibitor p21. After disruption of either the p53 or the p21 gene, gamma radiated cells progressed into mitosis and exhibited a G2 DNA content only because of a failure of cytokinesis. Thus, p53 and p21 appear to be essential for maintaining the G2 checkpoint in human cells.
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              Altered metabolite levels in cancer: implications for tumour biology and cancer therapy.

              Altered cell metabolism is a characteristic feature of many cancers. Aside from well-described changes in nutrient consumption and waste excretion, altered cancer cell metabolism also results in changes to intracellular metabolite concentrations. Increased levels of metabolites that result directly from genetic mutations and cancer-associated modifications in protein expression can promote cancer initiation and progression. Changes in the levels of specific metabolites, such as 2-hydroxyglutarate, fumarate, succinate, aspartate and reactive oxygen species, can result in altered cell signalling, enzyme activity and/or metabolic flux. In this Review, we discuss the mechanisms that lead to changes in metabolite concentrations in cancer cells, the consequences of these changes for the cells and how they might be exploited to improve cancer therapy.
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                Author and article information

                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                18 February 2019
                February 2019
                : 16
                : 4
                : 588
                Affiliations
                [1 ]Department of Earth and Sea Science, Laboratory of Marine Biochemistry and Ecotoxicology, University of Palermo, Via Barlotta 4, 91100 Trapani, Italy; simona.manuguerra@ 123456unipa.it (S.M.); cristobal.espinosaruiz@ 123456unipa.it (C.E.R.); andrea.santulli@ 123456unipa.it (A.S.)
                [2 ]Marine Biology Institute, Consorzio Universitario della Provincia di Trapani, Via Barlotta 4, 91100 Trapani, Italy
                Author notes
                [†]

                These two authors contributed equally to the work.

                Author information
                https://orcid.org/0000-0002-9542-2833
                https://orcid.org/0000-0002-3063-1634
                https://orcid.org/0000-0001-8089-5470
                https://orcid.org/0000-0003-3190-9420
                Article
                ijerph-16-00588
                10.3390/ijerph16040588
                6406823
                30781636
                80b37fca-bb1b-48cd-99dc-fe9a986ebc36
                © 2019 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
                : 07 January 2019
                : 14 February 2019
                Categories
                Article

                Public health
                pbdes,biomarkers,metabolism,oxidative stress,proliferation
                Public health
                pbdes, biomarkers, metabolism, oxidative stress, proliferation

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