1
40
5
-
Text
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URL Address
<a href="http://doi.org/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.etap.2018.12.019</a>
Pages
36–42
Volume
66
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Acute exposure to a glyphosate-containing herbicide formulation inhibits Complex II and increases hydrogen peroxide in the model organism Caenorhabditis elegans.
Publisher
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Environmental toxicology and pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
C. elegans; Glyphosate; Hydrogen peroxide; Mitochondrial inhibition; Oxygen consumption; Reactive oxygen species
Creator
An entity primarily responsible for making the resource
Burchfield Shelbie L; Bailey Denise C; Todt Callie E; Denney Rachel D; Negga Rekek; Fitsanakis Vanessa A
Description
An account of the resource
Glyphosate-based herbicides, such as Touchdown (TD) and Roundup, are among the most heavily-used herbicides in the world. While the active ingredient is generally considered non-toxic, the toxicity resulting from exposure to commercially-sold formulations is less clear. In many cases, cell cultures or various model organisms exposed to glyphosate formulations show toxicity and, in some cases, lethality. Using Caenorhabditis elegans, we assessed potential toxic mechanisms through which a highly-concentrated commercial formulation of TD promotes neurodegeneration. Following a 30-min treatment, we assayed mitochondrial electron transport chain function and reactive oxygen species (ROS) production. Initial oxygen consumption studies indicated general mitochondrial inhibition compared to controls ((*)p \textless 0.05). When Complex II activity was further assessed, inhibition was observed in all TD-treated groups ((*)p \textless 0.05). Complex IV activity, however, was not adversely affected by TD. This electron transport chain inhibition also resulted in reduced ATP levels ((*)p \textless 0.05). Furthermore, hydrogen peroxide levels, but not other ROS, were increased ((*)p \textless 0.05). Taken together, these data indicate that commercially-available formulations of TD may exert neurotoxicity through Complex II (succinate dehydrogenase) inhibition, decreased ATP levels, and increased hydrogen peroxide production.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">10.1016/j.etap.2018.12.019</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2019
Bailey Denise C
Burchfield Shelbie L
C. elegans
Denney Rachel D
Department of Pharmaceutical Sciences
Environmental toxicology and pharmacology
Fitsanakis Vanessa A
Glyphosate
Hydrogen peroxide
Mitochondrial inhibition
Negga Rekek
NEOMED College of Pharmacy
Oxygen Consumption
reactive oxygen species
Todt Callie E
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.etap.2018.12.019</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
36-42
Volume
66
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Acute exposure to a glyphosate-containing herbicide formulation inhibits Complex II and increases hydrogen peroxide in the model organism Caenorhabditis elegans.
Publisher
An entity responsible for making the resource available
Environmental toxicology and pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
C. elegans; Glyphosate; *hydrogen peroxide; Mitochondrial inhibition; Oxygen Consumption; *Reactive oxygen species; Animals; Reactive Oxygen Species/metabolism; Adenosine Triphosphate/metabolism; Herbicides/*toxicity; Caenorhabditis elegans/*drug effects/metabolism; Electron Transport Complex II/*antagonists & inhibitors/metabolism; Glycine/*analogs & derivatives/toxicity
Creator
An entity primarily responsible for making the resource
Burchfield Shelbie L; Bailey Denise C; Todt Callie E; Denney Rachel D; Negga Rekek; Fitsanakis Vanessa A
Description
An account of the resource
Glyphosate-based herbicides, such as Touchdown (TD) and Roundup, are among the most heavily-used herbicides in the world. While the active ingredient is generally considered non-toxic, the toxicity resulting from exposure to commercially-sold formulations is less clear. In many cases, cell cultures or various model organisms exposed to glyphosate formulations show toxicity and, in some cases, lethality. Using Caenorhabditis elegans, we assessed potential toxic mechanisms through which a highly-concentrated commercial formulation of TD promotes neurodegeneration. Following a 30-min treatment, we assayed mitochondrial electron transport chain function and reactive oxygen species (ROS) production. Initial oxygen consumption studies indicated general mitochondrial inhibition compared to controls ((*)p < 0.05). When Complex II activity was further assessed, inhibition was observed in all TD-treated groups ((*)p < 0.05). Complex IV activity, however, was not adversely affected by TD. This electron transport chain inhibition also resulted in reduced ATP levels ((*)p < 0.05). Furthermore, hydrogen peroxide levels, but not other ROS, were increased ((*)p < 0.05). Taken together, these data indicate that commercially-available formulations of TD may exert neurotoxicity through Complex II (succinate dehydrogenase) inhibition, decreased ATP levels, and increased hydrogen peroxide production.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">10.1016/j.etap.2018.12.019</a>
*hydrogen peroxide
*Reactive oxygen species
2019
Adenosine Triphosphate/metabolism
Animals
Bailey Denise C
Burchfield Shelbie L
C. elegans
Caenorhabditis elegans/*drug effects/metabolism
Denney Rachel D
Department of Pharmaceutical Sciences
Electron Transport Complex II/*antagonists & inhibitors/metabolism
Environmental toxicology and pharmacology
Fitsanakis Vanessa A
Glycine/*analogs & derivatives/toxicity
Glyphosate
Herbicides/*toxicity
Mitochondrial inhibition
Negga Rekek
NEOMED College of Pharmacy
Oxygen Consumption
Reactive Oxygen Species/metabolism
Todt Callie E
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.etap.2017.11.005" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.etap.2017.11.005</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
46-52
Volume
57
Search for Full-text
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<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Chronic exposure to a glyphosate-containing pesticide leads to mitochondrial dysfunction and increased reactive oxygen species production in Caenorhabditis elegans
Publisher
An entity responsible for making the resource available
Environmental Toxicology and Pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Subject
The topic of the resource
C. elegans; Glyphosate; Hydrogen peroxide; Mitochondrial inhibition; oxidative stress; Toxicology; Environmental Sciences & Ecology; Pharmacology & Pharmacy; parkinsons-disease; brain; alzheimers-disease; mechanisms; degeneration; species; neurodegenerative diseases; 6-ohda; C. elegans; complex-i; Herbicide; Reactive oxygen
Creator
An entity primarily responsible for making the resource
Bailey D C; Todt C E; Burchfield S L; Pressley A S; Denney R D; Snapp I B; Negga R; Traynor W L; Fitsanakis V A
Description
An account of the resource
Glyphosate-containing herbicides are among the most widely-used in the world. Although glyphosate itself is relatively non-toxic, growing evidence suggests that commercial herbicide formulations may lead to increased oxidative stress and mitochondrial inhibition. In order to assess these mechanisms in vivo, we chronically (24 h) exposed Caenorhabditis elegans to various concentrations of the glyphosate-containing herbicide TouchDown (TD). Following TD exposure, we evaluated the function of specific mitochondrial electron transport chain complexes. Initial oxygen consumption studies demonstrated inhibition in mid- and high-TD concentration treatment groups compared to controls. Results from tetramethylrhodamine ethyl ester and ATP assays indicated reductions in the proton gradient and ATP levels, respectively. Additional studies were designed to determine whether TD exposure resulted in increased reactive oxygen species (ROS) production. Data from hydrogen peroxide, but not superoxide or hydroxyl radical, assays showed statistically significant increases in this specific ROS. Taken together, these data indicate that exposure of Caenorhabditis elegans to TD leads to mitochondrial inhibition and hydrogen peroxide production.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.etap.2017.11.005" target="_blank" rel="noreferrer noopener">10.1016/j.etap.2017.11.005</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2018
6-ohda
alzheimers-disease
Bailey D C
Brain
Burchfield S L
C. elegans
complex-i
degeneration
Denney R D
Department of Pharmaceutical Sciences
Environmental Sciences & Ecology
Environmental toxicology and pharmacology
Fitsanakis V A
Glyphosate
Herbicide
Hydrogen peroxide
Journal Article or Conference Abstract Publication
mechanisms
Mitochondrial inhibition
Negga R
NEOMED College of Pharmacy
Neurodegenerative Diseases
Oxidative Stress
parkinsons-disease
Pharmacology & Pharmacy
Pressley A S
Reactive oxygen
Snapp I B
SPECIES
Todt C E
Toxicology
Traynor W L
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00401-019-02033-9</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Neurotoxicity of pesticides
Publisher
An entity responsible for making the resource available
Acta Neuropathologica
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-06
Subject
The topic of the resource
Dichlorodiphenyltrichloroethane; Dieldrin; Endosulfan; Fungicide; Glyphosate; iPSC; Microelectrode array; Mitochondrial Complex I; Neurodegeneration; Neurotoxicity; Organochlorine; Organophosphate; Paraquat; Pesticide; Pyrethroid; Pyridaben; Rotenone; Zebrafish
Creator
An entity primarily responsible for making the resource
Richardson Jason R; Fitsanakis Vanessa; Westerink Remco H S; Kanthasamy Anumantha G
Description
An account of the resource
Pesticides are unique environmental contaminants that are specifically introduced into the environment to control pests, often by killing them. Although pesticide application serves many important purposes, including protection against crop loss and against vector-borne diseases, there are significant concerns over the potential toxic effects of pesticides to non-target organisms, including humans. In many cases, the molecular target of a pesticide is shared by non-target species, leading to the potential for untoward effects. Here, we review the history of pesticide usage and the neurotoxicity of selected classes of pesticides, including insecticides, herbicides, and fungicides, to humans and experimental animals. Specific emphasis is given to linkages between exposure to pesticides and risk of neurological disease and dysfunction in humans coupled with mechanistic findings in humans and animal models. Finally, we discuss emerging techniques and strategies to improve translation from animal models to humans.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">10.1007/s00401-019-02033-9</a>
2019
Acta Neuropathologica
Department of Pharmaceutical Sciences
Dichlorodiphenyltrichloroethane
Dieldrin
Endosulfan
Fitsanakis Vanessa
Fungicide
Glyphosate
IPSC
June 2019 Update
Kanthasamy Anumantha G
Microelectrode array
Mitochondrial Complex I
NEOMED College of Pharmacy
Neurodegeneration
Neurotoxicity
Organochlorine
Organophosphate
Paraquat
Pesticide
Pyrethroid
Pyridaben
Richardson Jason R
Rotenone
Westerink Remco H S
Zebrafish
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00401-019-02033-9</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
343-362
Issue
3
Volume
138
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Neurotoxicity of pesticides.
Publisher
An entity responsible for making the resource available
Acta Neuropathologica
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-09
Subject
The topic of the resource
activity; cell-culture; developmental; Dichlorodiphenyltrichloroethane; Dieldrin; Endosulfan; exposure; Fungicide; Glyphosate; glyphosate-based herbicide; induced oxidative stress; iPSC; Microelectrode array; Mitochondrial Complex I; mitochondrial complex-i; Neurodegeneration; neuronal network; Neurosciences & Neurology; Neurotoxicity; Neurotoxicity; nigrostriatal dopamine system; Organochlorine; Organophosphate; Paraquat; parkinsons-disease; Pathology; Pesticide; Pyrethroid; pyrethroid insecticides; Pyridaben; reproduces features; Rotenone; Zebrafish
Creator
An entity primarily responsible for making the resource
Richardson Jason R; Fitsanakis Vanessa; Westerink Remco H S; Kanthasamy Anumantha G
Description
An account of the resource
Pesticides are unique environmental contaminants that are specifically introduced into the environment to control pests, often by killing them. Although pesticide application serves many important purposes, including protection against crop loss and against vector-borne diseases, there are significant concerns over the potential toxic effects of pesticides to non-target organisms, including humans. In many cases, the molecular target of a pesticide is shared by non-target species, leading to the potential for untoward effects. Here, we review the history of pesticide usage and the neurotoxicity of selected classes of pesticides, including insecticides, herbicides, and fungicides, to humans and experimental animals. Specific emphasis is given to linkages between exposure to pesticides and risk of neurological disease and dysfunction in humans coupled with mechanistic findings in humans and animal models. Finally, we discuss emerging techniques and strategies to improve translation from animal models to humans. [ABSTRACT FROM AUTHOR]
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">10.1007/s00401-019-02033-9</a>
2019
Acta Neuropathologica
activity
cell-culture
Department of Pharmaceutical Sciences
Developmental
Dichlorodiphenyltrichloroethane
Dieldrin
Endosulfan
exposure
Fitsanakis Vanessa
Fungicide
Glyphosate
glyphosate-based herbicide
induced oxidative stress
IPSC
Kanthasamy Anumantha G
Microelectrode array
Mitochondrial Complex I
mitochondrial complex-i
NEOMED College of Pharmacy
Neurodegeneration
neuronal network
Neurosciences & Neurology
Neurotoxicity
nigrostriatal dopamine system
Organochlorine
Organophosphate
Paraquat
parkinsons-disease
Pathology
Pesticide
Pyrethroid
pyrethroid insecticides
Pyridaben
reproduces features
Richardson Jason R
Rotenone
September 2019 Update
Westerink Remco H S
Zebrafish