Potential mechanisms of development-dependent adverse effects of the herbicide paraquat in 3D rat brain cell cultures

Sandström, Jenny; Broyer, A.; Zoia, Debora; Schilt, C.; Greggio, Chiara; Fournier, Margot; Q., Kim; Monnet‐Tschudi, Florianne

doi:10.1016/j.neuro.2017.04.010

Cited by 23 publications

(19 citation statements)

References 49 publications

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“…Neural tissue comprises several cell sub‐populations, so cell cultures containing all of them such as 3D rat brain cell cultures will reflect best the behavior of the neural tissue as a complex biological environment. This in vitro system consists of the major brain cell types –neurons, astrocytes, oligodendrocytes and microglia– and over the time, cultured cells undergo differentiation and maturation into a tissue‐like organization .…”

Section: Resultsmentioning

confidence: 99%

“…Cell aggregates from 3D rat neural cell cultures were obtained from the Department of Physiology of the University of Lausanne (Lausanne, Switzerland). Details on cell cultures can be found elsewhere . One hundred microliters of ice‐cold MeOH were added to an Eppendorf tube containing approximately 70 neurospheres, and then sonicated (3 × 4 s, 40% amplitude, Sonics Vibra‐Cell VCX 500, Sonics & Materials Inc., Newtown, CT, USA) for total disruption.…”

Section: Methodsmentioning

confidence: 99%

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Evolution in the design of a low sheath‐flow interface for CE‐MS and application to biological samples

et al. 2017

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Although several interfaces for CE-MS hyphenation are commercially available, the development of new versatile, simple and yet efficient and sensitive alternatives remains an important field of research. In a previous work, a simple low sheath-flow interface was developed from inexpensive parts. This interface features a design easy to build, maintain, and adapt to particular needs. The present work introduces an improved design of the previous interface. By reducing the diameter of the separation capillary and the emitter, a smaller Taylor cone is spontaneously formed, minimizing the zone dispersion while the analytes go through the interface and leading to less peak broadening associated to the ESI process. Numerical modeling allowed studying the mixing and diffusion processes taking place in the Taylor cone. The analytical performance of this new interface was tested with pharmaceutically relevant molecules and endogenous metabolites. The interface was eventually applied to the analysis of neural cell culture samples, allowing the identification of a panel of neurotransmission-related molecules. An excellent migration time repeatability was obtained (intra-day RSD <0.5% for most compounds, and <3.0% for inter-day precision). Most metabolites showed S/N ratios >10 with an injected volume of 6.7 nL of biological extract.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Evolution in the design of a low sheath‐flow interface for CE‐MS and application to biological samples

et al. 2017

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“…Given that catalase and an iron chelator attenuated cell death, the authors postulated that PQ-induced cell death was mediated in part via astrocyte-derived H 2 O 2 (Cantu, et al, 2009). In another study to elucidate the development-dependent effects of PQ, Sandstrom et al used 3D rat brain cultures to demonstrate that the perturbation of GSH-mediated defenses against oxidative stress and impairments in dopaminergic neurons were accompanied by stronger astrogliosis in immature cultures compared with mature cultures (Sandstrom, et al, 2017). The authors concluded that the increased vulnerability of immature cultures to the toxic effects of PQ might be attributed to insufficient protective mechanisms.…”

Section: Astrocytes and Paraquat-mentioning

confidence: 99%

Environmental neurotoxicant-induced dopaminergic neurodegeneration: a potential link to impaired neuroinflammatory mechanisms

Kanthasamy

Jin

Charli

et al. 2019

Pharmacology & Therapeutics

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With the increased incidence of neurodegenerative diseases worldwide, Parkinson's disease (PD) represents the second-most common neurodegenerative disease. PD is a progressive multisystem neurodegenerative disorder characterized by a marked loss of nigrostriatal dopaminergic neurons and the formation of Lewy pathology in diverse brain regions. Although the mechanisms underlying dopaminergic neurodegeneration remain poorly characterized, data from animal models and postmortem studies have revealed that heightened inflammatory responses mediated via microglial and astroglial activation and the resultant release of proinflammatory factors may act as silent drivers of neurodegeneration. In recent years, numerous studies have demonstrated a positive association between the exposure to environmental neurotoxicants and the etiology of PD. Although it is unclear whether neuroinflammation drives pesticide-induced neurodegeneration, emerging evidence suggests that the failure to dampen neuroinflammatory mechanisms may account for the increased vulnerability to pesticide neurotoxicity. Furthermore, recent studies provide additional evidence that shifts the focus from a neuron-centric view to glial-associated neurodegeneration following pesticide exposure. In this review, we propose to summarize briefly the possible factors that regulate neuroinflammatory processes during environmental neurotoxicant exposure with a focus on the potential roles of mitochondria-driven redox mechanisms. In this context, a critical discussion of the data obtained from experimental research and possible epidemiological studies is included. Finally, we hope to provide insights on the pivotal role of exosome-mediated intercellular transmission of aggregated proteins in microglial activation response and the resultant dopaminergic neurodegeneration after exposure to pesticides. Collectively, an improved understanding of glia-mediated neuroinflammatory signaling might provide novel insights into the mechanisms that contribute to neurodegeneration induced by environmental neurotoxicant exposure.

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“…Rotenone-induced neurotoxicity was less pronounced in neuron-enriched cultures than in neuron-glia cocultures , suggesting that neuron-glia interactions are critical for rotenone-induced neurodegeneration. In addition, in in vitro systems, a decrease in TH mRNA expression has been observed to be a sufficient signal to trigger microglial reactivity (Sandström et al, 2017). KE5 Neuroinflammation…”

Section: Moderatementioning

confidence: 99%

Adverse Outcome Pathway on Inhibition of the mitochondrial complex I of nigro-striatal neurons leading to parkinsonian motor deficits

Bal‐Price

Leist

Schildknecht

et al. 2018

OECD Series on Adverse Outcome Pathways

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Potential mechanisms of development-dependent adverse effects of the herbicide paraquat in 3D rat brain cell cultures

Cited by 23 publications

References 49 publications

Evolution in the design of a low sheath‐flow interface for CE‐MS and application to biological samples

Evolution in the design of a low sheath‐flow interface for CE‐MS and application to biological samples

Environmental neurotoxicant-induced dopaminergic neurodegeneration: a potential link to impaired neuroinflammatory mechanisms

Adverse Outcome Pathway on Inhibition of the mitochondrial complex I of nigro-striatal neurons leading to parkinsonian motor deficits

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