Summary of project PR001181

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 PR001181. The data can be accessed directly via it's Project DOI: 10.21228/M82418 This work is supported by NIH grant, U2C- DK119886.

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

Project ID: PR001181
Project DOI:doi: 10.21228/M82418
Project Title:Effects of Acute 2,3,7,8-Tetrachlorodibenzo-p-dioxin Exposure on the Circulating and Cecal Metabolome Profile
Project Type:Untargeted metabolomics
Project Summary:2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a polyhalogenated planar hydrocarbon belonging to a group of highly toxic and persistent environmental contaminants known as “dioxins”. TCDD is an animal teratogen and carcinogen that is well characterized for causing immunosuppression through activation of Aryl Hydrocarbon Receptor (AHR). In the current study, we investigated the effect of exposure of mice to an acute dose of TCDD on the metabolic profile within the serum and cecal contents to better define the effects of TCDD on host physiology. Our findings demonstrated that within the circulating metabolome following acute TCDD, there was significant dysregulation in the metabolism of bioactive lipids, amino acids, and carbohydrates when compared to the VEH treated mice. These wide-spread changes in metabolite abundance were identified to regulate host immunity via modulating Nuclear Factor-Kappa B (NF-κB) and Extracellular Signal‑Regulated Protein Kinase (ERK1/2) activity, and work as biomarkers for a variety of organ injuries and dysfunctions that follow TCDD exposure. Within the cecal content, of mice exposed to TCDD, we were able to detect changes in inflammatory markers that regulate NF-κB, markers of injury-related inflammation, and changes in lysine degradation, nicotinamide metabolism, and butanoate metabolism, which suggested an immediate suppression microbial metabolism. Collectively, these results demonstrate that acute TCDD exposure results in immediate irregularities in the circulating and intestinal metabolome which likely contributes to TCDD toxicity and can be used as biomarkers for the early detection of individual exposure.
Institute:University of South Carolina School of Medicine
Department:Department of Pathology
Laboratory:On behalf of Dr. Mitzi Nagarkatti Lab
Last Name:Lai
First Name:Yunjia
Address:1104 MHRC, 135 Dauer Dr., Chapel Hill, NC, 27599, USA
Email:yunjia.lai@outlook.com
Phone:9194805489
Funding Source:National Institute of Health: P01AT003961, P20GM103641, R01ES030144, R01AI129788 and R01AI123947
Project Comments:This is supporting metabolomics data for the publication in Chemosphere.
Publications:Chemosphere

Summary of all studies in project PR001181

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)
Release
Date
VersionSamplesDownload
(* : Contains raw data)
ST001871 Untargeted LC-MS metabolomics analysis of cecal content of mice treated with TCDD vs. vehicle control (part I) Mus musculus University of South Carolina School of Medicine MS* 2021-08-30 1 20 Uploaded data (6.6G)*
ST001872 Untargeted LC-MS metabolomics analysis of cecal content of mice treated with TCDD vs. vehicle control (part II) Mus musculus University of South Carolina School of Medicine MS* 2021-08-30 1 20 Uploaded data (5.8G)*
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