The role of gut microbiota in fetal methylmercury exposure: Insights from a pilot study

Sarah E. Rothenberg, Sharon Keiser, Nadim J. Ajami, Matthew C. Wong, Jonathan Gesell, Joseph F. Petrosino, Alexander Johs

Research output: Contribution to journalArticlepeer-review

59 Scopus citations

Abstract

Purpose: The mechanisms by which gut microbiota contribute to methylmercury metabolism remain unclear. Among a cohort of pregnant mothers, the objectives of our pilot study were to determine (1) associations between gut microbiota and mercury concentrations in biomarkers (stool, hair and cord blood) and (2) the contributions of gut microbial mercury methylation/demethylation to stool methylmercury. Methods: Pregnant women (36-39 weeks gestation, n = 17) donated hair and stool specimens, and cord blood was collected for a subset (n = 7). The diversity of gut microbiota was determined using 16S rRNA gene profiling (n = 17). For 6 stool samples with highest/lowest methylmercury concentrations, metagenomic whole genome shotgun sequencing was employed to search for the mercury methylation gene (hgcA), and two mer operon genes involved in methylmercury detoxification (merA and merB). Results: Seventeen bacterial genera were significantly correlated (increasing or decreasing) with stool methylmercury, stool inorganic mercury, or hair total mercury; however, aside from one genus, there was no overlap between biomarkers. There were no definitive matches for hgcA or merB, while merA was detected at low concentrations in all six samples. Major conclusions: Proportional differences in stool methylmercury were not likely attributed to gut microbiota through methylation/demethylation. Gut microbiota potentially altered methylmercury metabolism using indirect pathways.

Original languageEnglish
Pages (from-to)60-67
Number of pages8
JournalToxicology Letters
Volume242
DOIs
StatePublished - Feb 3 2016

Funding

This research was supported in part by grants to S.E. Rothenberg from the U.S. National Institute Of Environmental Health Sciences (Award: R15 ES022409 ), the U.S. National Institute of Health Loan Repayment Program (Awards: L30 ES023165 ), and the University of South Carolina Department of Environmental Health Sciences . This work was also supported in part by the U.S. Department of Energy Office of Science , Biological and Environmental Research , Subsurface Biogeochemical Research Program through grant DE SC0006809 to the Oak Ridge National Laboratory (ORNL) Mercury Scientific Focus Area. ORNL is managed by UT-Battelle, LLC under Contract No. DE-AC05-00OR22725 with the U.S. Department of Energy . By accepting the article for publication, the publisher acknowledges that the United States Government retains a non-exclusive, paid-up, irrevocable, worldwide license to publish or reproduce the published form of this manuscript, or allow others to do so, for United States Government purposes. The U.S. Department of Energy will provide public access to these results of federally sponsored research in accordance with the Public Access Plan ( http://energy.gov/downloads/doe-public-access-plan ). The content is solely the responsibility of the authors and does not necessarily represent the official views of the U.S. National Institutes of Health or the U.S. Department of Energy. The authors have no actual or potential conflicts of interest to report.

FundersFunder number
U.S. Department of Energy Office of Science
U.S. National Institute of Health Loan Repayment ProgramL30 ES023165
UT-Battelle, LLC
University of South Carolina Department of Environmental Health Sciences
National Institutes of Health
National Institute of Environmental Health SciencesR15ES022409
Biological and Environmental ResearchDE SC0006809
Oak Ridge National Laboratory

    Keywords

    • Gut microbiota
    • Mercury
    • Metabolism
    • Microbiome
    • Prenatal

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