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Event: 2263

Key Event Title

A descriptive phrase which defines a discrete biological change that can be measured. More help

Lysolecithin, increased

Short name

The KE short name should be a reasonable abbreviation of the KE title and is used in labelling this object throughout the AOP-Wiki. More help

LPS, increased

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Biological Context

Structured terms, selected from a drop-down menu, are used to identify the level of biological organization for each KE. More help

Level of Biological Organization
Cellular

Cell term

The location/biological environment in which the event takes place.The biological context describes the location/biological environment in which the event takes place. For molecular/cellular events this would include the cellular context (if known), organ context, and species/life stage/sex for which the event is relevant. For tissue/organ events cellular context is not applicable. For individual/population events, the organ context is not applicable. Further information on Event Components and Biological Context may be viewed on the attached pdf. More help

Organ term

Key Event Components

The KE, as defined by a set structured ontology terms consisting of a biological process, object, and action with each term originating from one of 14 biological ontologies (Ives, et al., 2017; https://aopwiki.org/info_pages/2/info_linked_pages/7#List). Biological process describes dynamics of the underlying biological system (e.g., receptor signalling).Biological process describes dynamics of the underlying biological system (e.g., receptor signaling). The biological object is the subject of the perturbation (e.g., a specific biological receptor that is activated or inhibited). Action represents the direction of perturbation of this system (generally increased or decreased; e.g., ‘decreased’ in the case of a receptor that is inhibited to indicate a decrease in the signaling by that receptor). Note that when editing Event Components, clicking an existing Event Component from the Suggestions menu will autopopulate these fields, along with their source ID and description. To clear any fields before submitting the event component, use the 'Clear process,' 'Clear object,' or 'Clear action' buttons. If a desired term does not exist, a new term request may be made via Term Requests. Event components may not be edited; to edit an event component, remove the existing event component and create a new one using the terms that you wish to add. Further information on Event Components and Biological Context may be viewed on the attached pdf. More help

Process	Object	Action
	lysophosphatidylcholine	increased

Key Event Overview

AOPs Including This Key Event

All of the AOPs that are linked to this KE will automatically be listed in this subsection. This table can be particularly useful for derivation of AOP networks including the KE.Clicking on the name of the AOP will bring you to the individual page for that AOP. More help

AOP Name	Role of event in AOP	Point of Contact	Author Status	OECD Status
Inhibition of NTE leading to delayed neuropathy via LPS cell membrane integration	KeyEvent	Brooke Bowe (send email)	Under development: Not open for comment. Do not cite
Inhibition of NTE leading to delayed neuropathy via increased inflammation	KeyEvent	Brooke Bowe (send email)	Under development: Not open for comment. Do not cite

Taxonomic Applicability

Latin or common names of a species or broader taxonomic grouping (e.g., class, order, family) that help to define the biological applicability domain of the KE.In many cases, individual species identified in these structured fields will be those for which the strongest evidence used in constructing the AOP was available in relation to this KE. More help

Term	Scientific Term	Evidence	Link
Homo sapiens	Homo sapiens		NCBI

Life Stages

An indication of the the relevant life stage(s) for this KE. More help

Sex Applicability

An indication of the the relevant sex for this KE. More help

Term	Evidence
Unspecific

Key Event Description

A description of the biological state being observed or measured, the biological compartment in which it is measured, and its general role in the biology should be provided. More help

LPC is a mixture of various fatty acid tails that are the hydrolysis products of phospholipids (McMurran, Zhao, & Franklin, 2019). LPC has been noted to be distributed along cell membranes of many cell types (Sato, 1973; Lee & Chan, 1977; McMurran, Zhao, & Franklin, 2019). It has numerous physiologic functions across tissues, including roles in receptor binding (particularly G protein-coupled receptors and Toll-like receptors), ion channel activation, and as a chemoattractant for inflammatory molecules (Liu, et al., 2020; Hachem & Nacir, 2022). In addition, LPC is known to be able to promote demyelination and as a result has been widely used in vitro to study certain neurodegenerative diseases such as multiple sclerosis and Alzheimer's disease (McMurran, Zhao, & Franklin, 2019; Liu, et al., 2020; Birgbauer, Rao, & Webb, 2004). LPC levels are regulated by the activity of numerous enzymes in the body. They are produced through phospholipase activity and eliminated by various lysophospholipases (Liu, et al., 2020; Quistad & Casida, 2004). Therefore, inhibition of some of these regulatory enzymes could cause alterations in the local concentration of LPC in tissues.

How It Is Measured or Detected

A description of the type(s) of measurements that can be employed to evaluate the KE and the relative level of scientific confidence in those measurements.These can range from citation of specific validated test guidelines, citation of specific methods published in the peer reviewed literature, or outlines of a general protocol or approach (e.g., a protein may be measured by ELISA). Do not provide detailed protocols. More help

Domain of Applicability

A description of the scientific basis for the indicated domains of applicability and the WoE calls (if provided). More help

References

List of the literature that was cited for this KE description. More help

Birgbauer, E., Rao, T. S., & Webb, M. (2004). Lysolecithin induces demyelination in vitro in a cerebellar slice culture system. Journal of Neuroscience Research, 78(2), 157-166.

Hachem, M., & Nacir, H. (2022). Emerging Role of Phospholipids and Lysophospholipids for Improving Brain Docosahexaenoic Acid as Potential Preventive and Therapeutic Strategies for Neurological Diseases. International Journal of Molecular Sciences, 23(7), 3969.

Lee, Y., & Chan, S. I. (1977). Effect of Lysolecithin on the Structure and Permeability of Lecithin Bilayer Vesicles. Biochemistry, 16(7), 1303-1309.

Liu, P., Zhu, W., Chen, C., Yan, B., Zhu, L., Chen, X., & Peng, C. (2020). The mechanisms of lysophosphatidylcholine in the development of diseases. Life Sciences, 247, 117443.

McMurran, C. E., Zhao, C., & Franklin, R. J. (2019). Toxin-Based Models to Investigate Demyelination and Remyelination. In D. A. Lyons, & L. Kegel, Oligodendrocytes: Methods and Protocols (pp. 377–396). Springer.

Quistad, G., & Casida, J. E. (2004). Lysophospholipase inhibition by organophosphorus toxicants. Toxicology and Applied Pharmacology, 196(3), 319-326.

Sato, T. (1973). Variability in the Lysolecithin Content of Human Erythrocyte Membranes. Chemical and Pharmaceutical Bulletin, 21(1), 176-183.