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      Effects of parental exposure to glyphosate-based herbicides on embryonic development and oxidative status: a long-term experiment in a bird model

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          Abstract

          Controversial glyphosate-based herbicides (GBHs) are the most frequently used herbicides globally. GBH residues are detected in soil, water, crops, and food products, potentially exposing non-target organisms to health risks; these organisms include wildlife, livestock, and humans. However, the potential for GBH-related parental effects are poorly understood. In the case of birds, GBHs may be transferred directly from mothers to eggs, or they may indirectly influence offspring performance by altered maternal resource allocation to eggs. We experimentally exposed a parental generation of Japanese quails ( Coturnix japonica) to GBHs (200 mg/kg feed) or respective controls. Glyphosate residues were found in eggs (ca 0.76 kg/mg). Embryonic development tended to be poorer in the eggs of GBH-exposed parents (76% of eggs showed normal development) compared to control parents (89% normal eggs). Embryonic brain tissue from GBH-exposed parents tended to express more lipid damage (20% higher), yet other biomarkers showed no apparent differences. We detected no differences in egg quality (egg, yolk, or shell mass, egg hormone concentration) across the treatment groups. Given this is the first long-term study testing parental effects of GBHs with birds, more studies are needed characterizing GBH-associated changes in maternal allocation and for example epigenetic programming.

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          Most cited references38

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          Environmental and health effects of the herbicide glyphosate

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            Potential toxic effects of glyphosate and its commercial formulations below regulatory limits.

            Glyphosate-based herbicides (GlyBH), including Roundup, are the most widely used pesticides worldwide. Their uses have increased exponentially since their introduction on the market. Residue levels in food or water, as well as human exposures, are escalating. We have reviewed the toxic effects of GlyBH measured below regulatory limits by evaluating the published literature and regulatory reports. We reveal a coherent body of evidence indicating that GlyBH could be toxic below the regulatory lowest observed adverse effect level for chronic toxic effects. It includes teratogenic, tumorigenic and hepatorenal effects. They could be explained by endocrine disruption and oxidative stress, causing metabolic alterations, depending on dose and exposure time. Some effects were detected in the range of the recommended acceptable daily intake. Toxic effects of commercial formulations can also be explained by GlyBH adjuvants, which have their own toxicity, but also enhance glyphosate toxicity. These challenge the assumption of safety of GlyBH at the levels at which they contaminate food and the environment, albeit these levels may fall below regulatory thresholds. Neurodevelopmental, reproductive, and transgenerational effects of GlyBH must be revisited, since a growing body of knowledge suggests the predominance of endocrine disrupting mechanisms caused by environmentally relevant levels of exposure.
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              Oxidative stress in neurodegenerative diseases.

              Oxidative stress refers to the cytopathologic consequences of a mismatch between the production of free radicals and the ability of the cell to defend against them. Growing data from experimental models and human brain studies suggest oxidative stress may play an important role in neuronal degeneration in diseases such as Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis. Mitochondrial oxidative metabolism, nitric oxide, phospholipid metabolism, and proteolytic pathways are potential sources of intracellular free radicals. Alterations in free radical defense systems may also contribute to oxidative stress. A net increase in reactive oxygen species can produce damage to lipids, proteins, and DNA and induce necrosis or apoptosis. Elucidating the pathways important in the production of and defense from free radicals may be important in devising new pharmacologic strategies to slow or halt neuronal degeneration.
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                Author and article information

                Contributors
                skruus@utu.fi
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                14 April 2020
                14 April 2020
                2020
                : 10
                : 6349
                Affiliations
                [1 ]ISNI 0000 0001 2097 1371, GRID grid.1374.1, Department of Biology, , University of Turku, ; Vesilinnantie 5, 20500 Turku, Finland
                [2 ]ISNI 0000 0001 2097 1371, GRID grid.1374.1, Biodiversity Unit, , University of Turku, ; Vesilinnantie 5, 20500 Turku, Finland
                Article
                63365
                10.1038/s41598-020-63365-1
                7156732
                32286465
                b0d3695a-5b0b-477b-a24a-06eabcbce84f
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 16 January 2020
                : 30 March 2020
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                © The Author(s) 2020

                Uncategorized
                developmental biology,ecology,physiology,zoology,environmental sciences
                Uncategorized
                developmental biology, ecology, physiology, zoology, environmental sciences

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