Multiple effects of the herbicide glufosinate-ammonium and its main metabolite on neural stem cells from the subventricular zone of newborn mice

Feat-Vetel, Justyne; Larrigaldie, Vanessa; Meyer-Dilhet, Géraldine; Herzine, Améziane; Mougin, Camille; Laugeray, Anthony; Gefflaut, Thierry; Richard, Olivier; Quesniaux, Valérie; Montécot-Dubourg, Céline; Mortaud, Stéphane

doi:10.1016/j.neuro.2018.10.001

Cited by 15 publications

(11 citation statements)

References 67 publications

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“…In this connection, Paraquat has been specifically shown to inhibit hippocampal neurogenesis in adult mice, as intraperitoneal administration of the compound for 3 weeks inhibited neural progenitor cell proliferation, altered developmental fate of newly generated cells in the hippocampus and impaired hippocampus-dependent learning and memory [153]. Perinatal exposure of the herbicide glufosinate-ammonium (GLA) to pregnant mothers inhibits SVG neurogenesis in newborn mice and altered the neuro-glial differentiation of cultured mouse primary neural stem cells [154,155]. Given the above connections between pesticides, adult neurogenesis and AD, it could be reasonably deduced that pesticide disruption or inhibition of adult neurogenesis may initiate or otherwise promote AD pathology.…”

Section: Effect On Adult Neurogenesismentioning

confidence: 99%

Neuropathological Mechanisms Associated with Pesticides in Alzheimer’s Disease

Tang

2020

Toxics

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Environmental toxicants have been implicated in neurodegenerative diseases, and pesticide exposure is a suspected environmental risk factor for Alzheimer’s disease (AD). Several epidemiological analyses have affirmed a link between pesticides and incidence of sporadic AD. Meanwhile, in vitro and animal models of AD have shed light on potential neuropathological mechanisms. In this paper, a perspective on neuropathological mechanisms underlying pesticides’ induction of AD is provided. Proposed mechanisms range from generic oxidative stress induction in neurons to more AD-specific processes involving amyloid-beta (Aβ) and hyperphosphorylated tau (p-tau). Mechanisms that are more speculative or indirect in nature, including somatic mutation, epigenetic modulation, impairment of adult neurogenesis, and microbiota dysbiosis, are also discussed. Chronic toxicity mechanisms of environmental pesticide exposure crosstalks in complex ways and could potentially be mutually enhancing, thus making the deciphering of simplistic causal relationships difficult.

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Section: Effect On Adult Neurogenesismentioning

confidence: 99%

Neuropathological Mechanisms Associated with Pesticides in Alzheimer’s Disease

Tang

2020

Toxics

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“…Un estudio realizado por Aris and Leblanc [32] encontró que un metabolito del GLA (ácido 3metilfosfinicopropiónico) podría detectarse en casi todas las muestras de suero sanguíneo de un grupo de pares madre-hijo, lo que indica una exposición universal y una potencial exposición transplacentaria. Aunque, la neurotoxicidad del GLA está bien documentada [31,33], los mecanismos subyacentes a través de los cuales GLA impactan el desarrollo del SNC siguen siendo desconocidos en gran parte. En este sentido, Dong, Guan [6] utilizaron un modelo animal de ratón para estudiar los efectos de la exposición prenatal del GLA.…”

Section: Glufosinato De Amoniounclassified

Residuos de plaguicidas y el trastorno del espectro autista

2021

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El trastorno del espectro autista (TEA) engloba a un conjunto de trastornos del neurodesarrollo que se caracterizan por una interacción social deficiente, comunicación restringida y comportamientos repetitivos y estereotipados. La etiología del TEA es desconocida a día de hoy, por lo que diversos equipos de investigación multidisciplinares están realizando grandes esfuerzos para intentar dilucidar los factores y mecanismos que intervienen en su aparición. En este sentido, existe un creciente interés en el estudio de factores ambientales como la exposición a residuos de plaguicidas ya que se dispone de suficiente evidencia científica sobre los efectos neurotóxicos que éstos pueden provocar. Por lo tanto, pueden ser formuladas hipótesis de asociaciones específicas entre el TEA y los residuos de plaguicidas. Este trabajo realiza una revisión sistemática sobre la influencia de la exposición a residuos de plaguicidas y la aparición del TEA. La metodología para llevar a cabo este trabajo de revisión sistemática siguió las directrices marcadas por el método PRISMA, encontrándose un total de siete artículos elegibles para su discusión. Los residuos de plaguicidas estudiados por los artículos seleccionados fueron los organofosforados y sus metabolitos; los organoclorados, incluidos el endosulfán y los bifenilos policlorados junto a sus metabolitos; los carbamatos; los piretroides, incluida la cipermetrina; y el glufosinato de amonio. El estudio de la acción de estos plaguicidas se centró en el periodo prenatal, investigándose su exposición en madres gestantes que vivían en zonas próximas a campos de cultivo donde se aplican pesticidas, en modelos animales de ratón y en cultivos de células cerebrales. Se encontró que existe relación entre la exposición a plaguicidas en el periodo prenatal y el riesgo de aparición de TEA en la descendencia junto a una disbiosis en la microbiota intestinal en ratones. Por lo tanto, es importante evaluar el factor de riesgo de exposición a residuos de plaguicidas en la aparición del TEA con más datos, para lo cual se requieren más estudios tanto in vitro como in vivo con el fin de dilucidar los mecanismos bioquímicos precisos involucrados.

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“…Rising use has been driven by the spread of weeds that have become resistant to onceeffective herbicides, especially glyphosate. Each of these four herbicides is associated with combinations of reproductive risks [7,[38][39][40][41], birth defects [42][43][44][45][46][47][48], and cancer [49][50][51][52][53].…”

Section: Accuracy and Limits Of The Dri Systemmentioning

confidence: 99%

The dietary risk index system: a tool to track pesticide dietary risks

Benbrook¹,

Davis

2020

Environ Health

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Background For years the United States Department of Agriculture’s Pesticide Data Program and the United Kingdom’s Food Standards Agency have published annual or quarterly data on pesticide residues in foods. Both programs report residues in conventionally grown, organic, and imported foods. The US program has tested about 288,000 food samples since 1992, primarily fruits and vegetables consumed by children. Since 1999 the UK has tested about 72,000 samples of a wider range of foods. These data are vital inputs in tracking trends in pesticide dietary risks. Methods The Dietary Risk Index (DRI) system facilitates detailed analyses of US and UK pesticide residue data, trends, and chronic risk distributions. The DRI value for a pesticide is the dietary intake of that pesticide from a single serving of food divided by the pesticide’s acceptable daily intake as set by the US Environmental Protection Agency. It can be calculated based on average annual residue concentrations, and on residue levels in individual samples of food. DRI values can be aggregated over multiple pesticides in single foods, and over individual pesticides in multiple foods. Results The DRI system provides insights into the levels, trends, and distribution of pesticide dietary risk across most widely consumed foods. By drawing on both US Pesticide Data Program and UK-Food Standards Agency residue data, the DRI is capable of assessing pesticide risks in a significant portion of the global food supply. Substantial reductions in pesticide dietary risks occurred in the early 2000s, primarily from replacement of organophosphate insecticides with seemingly lower-risk neonicotinoids. However, there remain several areas of concern and opportunities to reduce risks. Both herbicide and fungicide dietary risks are rising. Organically grown produce poses risks far lower than corresponding, conventionally grown produce. Risk differences are inconsistent between domestic and imported foods. Conclusions The surest ways to markedly reduce pesticide dietary risks are to shift relatively high-risk fruits and vegetables to organic production. For other foods, reducing reliance on pesticides overall, and especially high-risk pesticides, will incrementally lower risks. The DRI system can help focus such efforts and track progress in reducing pesticide dietary risk.

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Multiple effects of the herbicide glufosinate-ammonium and its main metabolite on neural stem cells from the subventricular zone of newborn mice

Cited by 15 publications

References 67 publications

Neuropathological Mechanisms Associated with Pesticides in Alzheimer’s Disease

Neuropathological Mechanisms Associated with Pesticides in Alzheimer’s Disease

Residuos de plaguicidas y el trastorno del espectro autista

The dietary risk index system: a tool to track pesticide dietary risks

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