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    Analyzing the Effects of Mercury on Acetylcholinesterase In Vitro

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    http://hdl.handle.net/11603/25283
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    Author/Creator
    Strange, Jessica
    Date
    2022-06
    Type of Work
    55 pages
    Text
    theses
    Department
    Biological Sciences
    Program
    Master of Science in Applied Biology
    Subjects
    Mercury
    Acetylcholinesterase
    AChE
    Inflammatory response
    Mercury -- Health aspects
    Cholinergic anti-inflammatory pathway
    Abstract
    This study aims to establish a viable method for testing the relationship between low doses of inorganic mercury and the enzyme acetylcholinesterase (AChE) in vitro. Mercury has been identified as a heavy metal that can induce an immune response through cytokine signaling, resulting in an unopposed inflammatory response by downregulating the production of anti-inflammatory cytokines. The ubiquity of mercury as an environmental toxicant and its ability to bioaccumulate and become biomagnified makes it a xenobiotic of interest in many toxicological studies. This is notably performed in concentrations of micromolar ranges or higher. Previous findings support a dysregulation of the immune response when mercury exposure occurring in the nanomolar range is coupled with bacterial or viral adjuncts. This co-exposure is demonstrated exasperating the effects seen in the inflammatory response through the inhibition of the anti-inflammatory counteraction of the immune system to reestablish homeostasis. The further understanding of the cholinergic anti-inflammatory pathway (CAP) and the enzyme AChE as a regulator is one area of interest when hypothesizing the mechanism of this inflammatory response. This research presented in this manuscript establishes the use of a continuous assay based on Ellman’s method as a viable method to assess the effects of mercury on AChE in vitro which allows for the further analysis of this complex relationship between low dose mercury exposures, bacterial adjuncts, and the CAP. Specifically, this method offers an explanation for a potential mechanism of how these components relate to one another and the upregulation of the inflammatory response, and specifically how it becomes unchallenged.


    Salisbury University
    Guerrieri Academic Commons
    1101 Camden Ave.
    Salisbury, MD 21801

    www.salisbury.edu

    Contact Information:
    Email: SOAR@salisbury.edu
    Phone: 410.543.6206


    If you wish to submit a copyright complaint or withdrawal request, please email mdsoar-help@umd.edu.

     

     

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    Salisbury University
    Guerrieri Academic Commons
    1101 Camden Ave.
    Salisbury, MD 21801

    www.salisbury.edu

    Contact Information:
    Email: SOAR@salisbury.edu
    Phone: 410.543.6206


    If you wish to submit a copyright complaint or withdrawal request, please email mdsoar-help@umd.edu.