Summary of Study ST004274

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 PR002700. The data can be accessed directly via it's Project DOI: 10.21228/M8NK11 This work is supported by NIH grant, U2C- DK119886. See: https://www.metabolomicsworkbench.org/about/howtocite.php

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Study IDST004274
Study TitleLoss of vitamin C biosynthesis protects from the pathology of a Schistosome infection and egg production.
Study TypeTreatment experiment
Study SummaryThe processes influenced by ascorbate treatment in schistosome reproduction were investigated by metabolomics analysis of Ascorbate-treated and -untreated worm samples in the culture media. The top metabolite enriched in ascorbate-treated schistosomes was L-DOPA, a product of tyrosinase activity, which crosslinks vitellocyte proteins to form the schistosome eggshell, consistent with a role for ascorbate in vitellocyte development.
Institute
University of Texas Southwestern Medical Center at Dallas
DepartmentChildren’s Medical Center Research Institute
LaboratoryMichalis Agathokleous
Last NameAgathokleous
First NameMichalis
Address6000 Harry Hines Blvd, NL12.110N, Dallas, TX, 75235
Emailmichail.agathokleous@utsouthwestern.edu
Phone2146486270
Submit Date2025-10-06
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailLC-MS
Release Date2025-10-31
Release Version1
Michalis Agathokleous Michalis Agathokleous
https://dx.doi.org/10.21228/M8NK11
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR002700
Project DOI:doi: 10.21228/M8NK11
Project Title:Loss of vitamin C biosynthesis protects from the pathology of a Schistosome infection
Project Type:MS quantitative analysis
Project Summary:Schistosoma parasite is known to require ascorbate to produce eggs in vitro culture. To investigate the effect of ascorbate deficiency in mice infected with Schistosoma mansoni, the pathology of infection was analyzed in vivo. S. mansoni required host ascorbate to produce eggs and consequently, ascorbate-deficient mice were protected from schistosomiasis pathologies including liver granuloma formation and transmission. To understand the processes dependent on ascorbate metabolome and gene expression profiles were compared between Ascorbate-treated and -untreated samples. Our work shows that ascorbate deficiency can have physiological benefits by protecting animals from the pathology of a major parasitic disease.
Institute:UT Southwestern Medical Center
Department:CRI
Laboratory:Michalis Agathokleous
Last Name:Agathokleous
First Name:Michalis
Address:5323 Harry Hines Blvd, Children's Research Institute, Dallas, TX, 75309, USA
Email:michail.agathokleous@utsouthwestern.edu
Phone:2146486270
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