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Role of microbial microbes in arsenic bioaccumulation and biotransformation in mice.

Authors :
Huang L
Ye Z
Zhao Q
Li Y
Yu ZG
Zhang W
Source :
Toxicology and applied pharmacology [Toxicol Appl Pharmacol] 2023 Apr 01; Vol. 464, pp. 116447. Date of Electronic Publication: 2023 Mar 07.
Publication Year :
2023

Abstract

Although gut microbes can affect the accumulation and metabolism of arsenic (As), the microbes contributing to these processes remain largely unknown. Therefore, this study aimed to investigate the bioaccumulation and biotransformation of arsenate [As(V)] and arsenobetaine (AsB) in mice with a disordered gut microbiome. We used cefoperazone (Cef) to construct a mouse model of gut microbiome disruption along with 16S rRNA sequencing to elucidate the effect of gut microbiome destruction on the biotransformation and bioaccumulation of As(V) and AsB. This revealed the role of specific bacteria in As metabolism. Gut microbiome destruction increased the bioaccumulation of As(V) and AsB in various organs and reduced the excretion of As(V) and AsB in the feces. Further, gut microbiome destruction was found to be important for the biotransformation of As(V). Interference with Cef can significantly decrease Blautia and Lactobacillus while increasing Enterococcus, leading to increase As accumulation in mice and enhanced methylation. We also identified Lachnoclostridium, Erysipelatoclostridium, Blautia, Lactobacillus, and Enterococcus as biomarkers involved in As bioaccumulation and biotransformation. In conclusion, specific microbes can increase As accumulation in the host, exacerbating its potential health risks.<br />Competing Interests: Declaration of Competing Interest The authors declare no competing interests to report.<br /> (Copyright © 2023 Elsevier Inc. All rights reserved.)

Details

Language :
English
ISSN :
1096-0333
Volume :
464
Database :
MEDLINE
Journal :
Toxicology and applied pharmacology
Publication Type :
Academic Journal
Accession number :
36889513
Full Text :
https://doi.org/10.1016/j.taap.2023.116447