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      Desreguladores endócrinos no meio ambiente: efeitos e conseqüências Translated title: Endocrine disrupters in the enviroment: part 1 - effects and consequences

      research-article
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      Química Nova
      Sociedade Brasileira de Química
      Endocrine Disrupting Chemicals, environment, human health

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          Translated abstract

          There is an increasing interest in micropollutants in the environment that can interfere with the endocrine system, affecting health, growth and reproduction of animals and humans. These substances are known as Endocrine Disrupting Chemicals (EDCs) and can be found in domestic sewage, domestic wastewater treatment plant effluents, and in natural and potable waters. There are numerous chemicals classified as EDCs, such as pesticides, chemicals used and produced by chemical industries and natural and synthetic estrogens. EDCs can be related to the increase of the incidence of anomalies in the reproductive system of animals, cancer in humans and reduction of the masculine fertility.

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          Most cited references15

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          Pesticides and Parkinson’s Disease—Is There a Link?

          Parkinson’s disease (PD) is an idiopathic disease of the nervous system characterized by progressive tremor, bradykinesia, rigidity, and postural instability. It has been postulated that exogenous toxicants, including pesticides, might be involved in the etiology of PD. In this article we present a comprehensive review of the published epidemiologic and toxicologic literature and critically evaluate whether a relationship exists between pesticide exposure and PD. From the epidemiologic literature, there does appear to be a relatively consistent relationship between pesticide exposure and PD. This relationship appears strongest for exposure to herbicides and insecticides, and after long durations of exposure. Toxicologic data suggest that paraquat and rotenone may have neurotoxic actions that potentially play a role in the development of PD, with limited data for other pesticides. However, both the epidemiology and toxicology studies were limited by methodologic weaknesses. Particular issues of current and future interest include multiple exposures (both pesticides and other exogenous toxicants), developmental exposures, and gene–environment interactions. At present, the weight of evidence is sufficient to conclude that a generic association between pesticide exposure and PD exists but is insufficient for concluding that this is a causal relationship or that such a relationship exists for any particular pesticide compound or combined pesticide and other exogenous toxicant exposure.
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            Raw Single-Wall Carbon Nanotubes Induce Oxidative Stress and Activate MAPKs, AP-1, NF-κB, and Akt in Normal and Malignant Human Mesothelial Cells

            Background Single-wall carbon nanotubes (SWCNTs), with their unique physicochemical and mechanical properties, have many potential new applications in medicine and industry. There has been great concern subsequent to preliminary investigations of the toxicity, biopersistence, pathogenicity, and ability of SWCNTs to translocate to subpleural areas. These results compel studies of potential interactions of SWCNTs with mesothelial cells. Objective Exposure to asbestos is the primary cause of malignant mesothelioma in 80–90% of individuals who develop the disease. Because the mesothelial cells are the primary target cells of asbestos-induced molecular changes mediated through an oxidant-linked mechanism, we used normal mesothelial and malignant mesothelial cells to investigate alterations in molecular signaling in response to a commercially manufactured SWCNT. Methods In the present study, we exposed mesothelial cells to SWCNTs and investigated reactive oxygen species (ROS) generation, cell viability, DNA damage, histone H2AX phosphorylation, activation of poly(ADP-ribose) polymerase 1 (PARP-1), stimulation of extracellular signal-regulated kinase (ERKs), Jun N-terminal kinases (JNKs), protein p38, and activation of activator protein-1 (AP-1), nuclear factor κB (NF-κB), and protein serine-threonine kinase (Akt). Results Exposure to SWCNTs induced ROS generation, increased cell death, enhanced DNA damage and H2AX phosphorylation, and activated PARP, AP-1, NF-κB, p38, and Akt in a dose-dependent manner. These events recapitulate some of the key molecular events involved in mesothelioma development associated with asbestos exposure. Conclusions The cellular and molecular findings reported here do suggest that SWCNTs can cause potentially adverse cellular responses in mesothelial cells through activation of molecular signaling associated with oxidative stress, which is of sufficient significance to warrant in vivo animal exposure studies.
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              Environ. Health Perspect.

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                Author and article information

                Journal
                qn
                Química Nova
                Quím. Nova
                Sociedade Brasileira de Química (São Paulo, SP, Brazil )
                0100-4042
                1678-7064
                June 2007
                : 30
                : 3
                : 651-666
                Affiliations
                [01] Rio de Janeiro RJ orgnameUniversidade Federal do Rio de Janeiro orgdiv1Programas de Pós-graduação de Engenharia Brasil
                Article
                S0100-40422007000300027 S0100-4042(07)03000327
                10.1590/S0100-40422007000300027
                9e2c0669-741c-4c0a-8326-0747bb43bf36

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 21 March 2006
                : 21 July 2006
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 161, Pages: 16
                Product

                SciELO Brazil

                Categories
                Revisão

                human health,environment,Endocrine Disrupting Chemicals

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