Society of Toxicology Develops Learning Framework for Undergraduate Toxicology Courses Following the Vision and Change Core Concepts Model.
The Society of Toxicology announces the development of a Learning Framework (https://www.toxicology.org/education/docs/SOT-Toxicology-Learning-Objectives.pdf ) for undergraduate toxicology that will facilitate the development and sharing of evidence-based teaching materials for undergraduate toxicology educators throughout the world. This Learning Framework was modeled on the "Vision and Change Report" (www.visionandchange.org), an effort of the National Science Foundation and American Association for the Advancement of Science defining Core Concepts and Core Competencies to inform undergraduate biology course design. Vision and Change (V&C) has gained national acceptance, becoming a foundation for 14 upper-level courses designed by professional life science scientific societies. The undergraduate toxicology Learning Framework includes five Core Concepts aligned with V&C that encompass the discipline of toxicology: Evolution; Biological Information, Risk and Risk; Management; Systems Toxicology; and Pathways and Transformations for Energy and Matter. Underpinning the Core Concepts are Level Two Toxicology Concepts, which are broad disciplinary categories, Level Three Learning Objectives, which address specific learning goals, and Level Four Example Learning Objectives and Case Studies, which provide examples of how content might be taught. Syllabi from more than 20 undergraduate toxicology courses and several undergraduate toxicology textbooks were surveyed to determine toxicology-related Learning Objectives. From these, undergraduate educators can design courses tailored to their institutional needs by selecting a subset of Learning Objectives. Publication of a Learning Framework for toxicology will enable integration into other disciplines and facilitate the development and sharing of evidenced-based teaching materials for toxicology to educators in allied disciplines. Ultimately this will expand toxicology's impact to a broader audience.
Gray Joshua P; Curran Christine P; Fitsanakis Vanessa A; Ray Sidhartha; Stine Karen E; Eidemiller Betty J
Toxicological sciences : an official journal of the Society of Toxicology
2019
2019-04
<a href="http://doi.org/10.1093/toxsci/kfz090" target="_blank" rel="noreferrer noopener">10.1093/toxsci/kfz090</a>
Acute exposure to a glyphosate-containing herbicide formulation inhibits Complex II and increases hydrogen peroxide in the model organism Caenorhabditis elegans.
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
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.
Burchfield Shelbie L; Bailey Denise C; Todt Callie E; Denney Rachel D; Negga Rekek; Fitsanakis Vanessa A
Environmental toxicology and pharmacology
2019
2019-02
<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>
Acute exposure to a glyphosate-containing herbicide formulation inhibits Complex II and increases hydrogen peroxide in the model organism Caenorhabditis elegans.
C. elegans; Glyphosate; Hydrogen peroxide; Mitochondrial inhibition; Oxygen consumption; Reactive oxygen species
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.
Burchfield Shelbie L; Bailey Denise C; Todt Callie E; Denney Rachel D; Negga Rekek; Fitsanakis Vanessa A
Environmental toxicology and pharmacology
2019
2019-02
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<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>