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      Neuropsychiatric Disease and Treatment (submit here)

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      Effects of prenatal exposure to temephos on behavior and social interaction

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          Abstract

          The neurodevelopment period is susceptible to alterations by genetic and environmental factors, such as the exposure to organophosphates (OP). The OP is neurotoxic and has been associated with neurological diseases pathophysiology. The OP temephos is widely used against Aedes aegypti in Brazil’s public health programs.

          Purpose

          To evaluate behavioral effects of prenatal exposition to temephos in Wistar rats.

          Methods

          First, we divided pregnant females into groups: those who received temephos diluted in distilled water by gavage between gestational days 6–13 and those who received only distilled water in the same period and volume. Then, we divided pups according to sex and exposure, and we made the behavioral tests on postnatal day 30.

          Results

          Prenatal exposure to temephos caused hyperactivity, stereotyped behavior, and social impairment in animals.

          Conclusion

          These results are similar to the altered behavior presented in some neurobiological diseases models, like Attention Deficit Hyperactivity Disorder and Autism Spectrum Disorders, and this study may bring a red alert to the large use of temephos in Brazil, due to the damage caused by its exposure.

          Most cited references25

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          Emotional behavior in the rat. I. Defecation and urination as measures of individual differences in emotionality.

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            Cholinergic systems in brain development and disruption by neurotoxicants: nicotine, environmental tobacco smoke, organophosphates.

            Acetylcholine and other neurotransmitters play unique trophic roles in brain development. Accordingly, drugs and environmental toxicants that promote or interfere with neurotransmitter function evoke neurodevelopmental abnormalities by disrupting the timing or intensity of neurotrophic actions. The current review discusses three exposure scenarios involving acetylcholine systems: nicotine from maternal smoking during pregnancy, exposure to environmental tobacco smoke (ETS), and exposure to the organophosphate insecticide, chlorpyrifos (CPF). All three have long-term, adverse effects on specific processes involved in brain cell replication and differentiation, synaptic development and function, and ultimately behavioral performance. Many of these effects can be traced to the sequence of cellular events surrounding the trophic role of acetylcholine acting on its specific cellular receptors and associated signaling cascades. However, for chlorpyrifos, additional noncholinergic mechanisms appear to be critical in establishing the period of developmental vulnerability, the sites and type of neural damage, and the eventual outcome. New findings indicate that developmental neurotoxicity extends to late phases of brain maturation including adolescence. Novel in vitro and in vivo exposure models are being developed to uncover heretofore unsuspected mechanisms and targets for developmental neurotoxicants.
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              Organophosphate pesticide exposure and neurodegeneration.

              Organophosphate pesticides (OPs) are used extensively throughout the world. The main sources of contamination for humans are dietary ingestion and occupational exposures. The major concerns related to OP exposure are delayed effects following high level exposures as well as the impact of low level exposures during the lifespan which are suggested to be a risk factor for nervous system chronic diseases. Both high and low level exposures may have a particularly high impact in population subgroups such as aged or genetically vulnerable populations. Apart from the principle action of OPs which involves inhibition of the acetylcholinesterase (AChE) enzyme, several molecular targets, such as hormones; neurotransmitters; neurotrophic factors; enzymes related to the metabolism of beta amyloid protein as well as inflammatory changes have been identified for OP compounds. Here we review the main neurological and/or cognitive deficits described and the experimental and epidemiological relationships found between pesticide exposure and Alzheimer's, Parkinson's, and Amyotrophic Lateral Sclerosis (ALS) diseases. This report also focuses on possible individual differences making groups resilient or vulnerable to these toxicants. A critical discussion of the evidence obtained from experimental models and possible sources of bias in epidemiological studies is included. In particular this review aims to discuss common targets and pathways identified which may underlie the functional deficits associated with both pesticide exposure and neurodegeneration.
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                Author and article information

                Journal
                Neuropsychiatr Dis Treat
                Neuropsychiatr Dis Treat
                Neuropsychiatric Disease and Treatment
                Neuropsychiatric Disease and Treatment
                Dove Medical Press
                1176-6328
                1178-2021
                2019
                11 March 2019
                : 15
                : 669-673
                Affiliations
                [1 ]Neurobiology Laboratory of Inflammatory and Metabolic Processes, University of Southern Santa Catarina, Tubarão, Santa Catarina, Brazil, fabiana.durante@ 123456gmail.com
                [2 ]Postgraduate Program in Health Sciences, University of Southern Santa Catarina, Tubarão, Santa Catarina, Brazil
                Author notes
                Correspondence: Fabiana Durante de Medeiros, Neurobiology Laboratory of Inflammatory and Metabolic Processes, University of Southern Santa Catarina, Av. José Acácio Moreira, 787, Dehon, Tubarão, Santa Catarina 88704-900, Brazil, Tel +55 48 3621 3192; +55 489 9906 5383, Email fabiana.durante@ 123456gmail.com
                Article
                ndt-15-669
                10.2147/NDT.S193896
                6417020
                863a5dba-8066-4702-9e90-85b41a6d7afe
                © 2019 Martins Laurentino et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Neurology
                neurodevelopment,organophosphate,toxicity,temephos
                Neurology
                neurodevelopment, organophosphate, toxicity, temephos

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