Summary of Study ST002800

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001747. The data can be accessed directly via it's Project DOI: 10.21228/M8WH9J This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002800
Study TitleHepatic oxylipin profiles in mouse models of Wilson disease: new insights into early hepatic manifestations.
Study SummaryHepatic inflammation is commonly identified in Wilson disease (WD), a genetic disease of hepatic and brain copper accumulation. Copper accumulation is associated with increased reactive oxygen species and activation of the non-enzymatic oxidation of membrane-bound polyunsaturated fatty acids (PUFA), with impairment of cellular structures and function. Products of PUFA oxidation are collectively known as oxylipins (OXL), which can also be produced via enzymatic pathways including lipoxygenases (LOXs), cyclooxygenases (COXs), and cytochrome P450 monooxygenases (CYPs). These bioactive lipids modulate hepatic inflammation. We aimed to examine hepatic OXLs profile at early stages of WD in mouse model of Wilson disease, the toxic milk from The Jackson Laboratory (tx-j) compared to mice with normal copper metabolism (C3H). Targeted lipidomic profiling of OXLs was performed by ultra-high-performance liquid chromatography-electrospray ionization-tandem mass spectrometry (UPLC-ESI-MS/MS) in livers from 16 weeks old male and female mice. Hepatic OXL profiles were altered, with higher levels of PUFA alcohols, diols, and ketones. Markers of oxidative stress, 9-HETE and 9-HEPE were increased in tx-j mice. Hepatic prostaglandin and thromboxane levels in the COX pathway were increased in tx-j mice. tx-j showed altered PUFA-epoxides, suggesting altered CYP(s) activities. Our findings suggest that both non-enzymatic ROS-dependent and enzymatic PUFAs oxidation via COX and LOX pathways are associated with early stages liver disease in WD. It also indicates altered CYPs activities in animal model of WD. These novel pathways could be the target for future therapies.
Institute
University of California, Davis
Last NameSarode
First NameGaurav
AddressGenome & Biomedical Sciences Facility, 451 E. Health Sciences Dr., Davis, CA, 95616, USA
Emailgsarode@ucdavis.edu
Phone530752-6715
Submit Date2023-07-18
Raw Data AvailableYes
Raw Data File Type(s)wiff
Analysis Type DetailLC-MS
Release Date2024-01-18
Release Version1
Gaurav Sarode Gaurav Sarode
https://dx.doi.org/10.21228/M8WH9J
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id Treatment
SA300730930C3H 5001
SA300731928C3H 5001
SA300732926C3H 5001
SA300733900C3H 5001
SA300734927C3H 5001
SA300735929C3H 5001
SA300736906C3H 5001
SA300737901C3H 5001
SA300738903C3H 5001
SA300739902C3H 5001
SA300740905C3H 5001
SA300741904C3H 5001
SA300742922tx-J 5001
SA300743921tx-J 5001
SA300744923tx-J 5001
SA300745924tx-J 5001
SA300746920tx-J 5001
SA300747925tx-J 5001
SA300748916tx-J 5001
SA300749911tx-J 5001
SA300750910tx-J 5001
SA300751909tx-J 5001
SA300752908tx-J 5001
SA300753912tx-J 5001
SA300754913tx-J 5001
SA300755918tx-J 5001
SA300756917tx-J 5001
SA300757915tx-J 5001
SA300758914tx-J 5001
SA300759919tx-J 5001
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