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 ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : 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)* |
