Full length article
The gut microbiome promotes arsenic metabolism and alleviates the metabolic disorder for their mammal host under arsenic exposure

https://doi.org/10.1016/j.envint.2022.107660Get rights and content
Under a Creative Commons license
open access

Highlights

  • Normal gut microbiome and metabolics contributes to the fecal arsenic excretion and biotransformation.

  • Normal gut microbiome decreases the liver accumulation.

  • Normal gut microbiome withstands arsenic stress by maintain a healthier fecal microbial networks and healthier fecal metabolome including amino acids, short chain fatty acids, organic acids and bile acid.

  • Normal gut microbiome can and alleviated the metabolic disorder of the mammal host under arsenic exposure.

Abstract

Gut microbiome can participate in arsenic metabolism. However, its efficacy in the host under arsenic stress is still controversial. To clarify their roles in fecal arsenic excretion, tissue arsenic accumulation, host physiological states and metabolism, in this study, ninety-six C57BL/6 male mice were randomly divided to four groups, groups A and B were given sterile water, and groups C and D were given the third generation of broad-spectrum antibiotic (ceftriaxone) to erase the background gut microbiome. Subsequently, groups B and D were subchronicly exposed to arsenic containing feed prepared by adding arsenical mixture (rice arsenic composition) into control feed. In group D, the fecal total arsenic (CtAs) decreased by 25.5 %, iAsIII composition increased by 46.9 %, unclarified As (uAs) composition decreased by 92.4 %, and the liver CtAs increased by 26.7 %; the fecal CtAs was positively correlated with microbial richness and some metabolites (organic acids, amino acids, carbohydrates, SCFAs, hydrophilic bile acids and their derivatives); and fecal DMA was positively correlated with microbial richness and some metabolites (ferulic acid, benzenepropanoic acid and pentanoic acid); network analysis showed that the numbers of modules, nodes, links were decreased and vulnerability was increased; some SCFAs and hydrophilic bile acid decreased, and hydrophobic bile acids increased (Ps < 0.05). In the tissue samples of group D, Il-18 and Ifn-γ gene expression increased and intestinal barrier-related genes Muc2, Occludin and Zo-1 expression decreased (Ps < 0.05); serum glutathione and urine malondialdehyde significantly increased (Ps < 0.05); urine metabolome significantly changed and the variation was correlated with six SCFAs-producing bacteria, and some SCFAs including isobutyric acid, valeric acid and heptanoic acid decreased (Ps < 0.05). Therefore, the normal gut microbiome increases fecal arsenic excretion and biotransformation, which can maintain a healthier microbiome and metabolic functions, and alleviate the metabolic disorder for their mammal host under arsenic exposure.

Keywords

Rice arsenicals
Arsenic biotransformation
Gut microbiome
Metabolomics
Ceftriaxone

Abbreviations

ICP-MS
Inductively Coupled Plasma-Mass Spectrometry
HPLC-ICP-MS
High Performance Liquid Chromatography-Inductively Coupled Plasma-Mass Spectrometry
UPLC-MS
Ultra Performance Liquid Chromatography-Mass Spectrometry
GC–MS
Gas Chromatographic Mass Spectrometry
SRA
Sequence Read Archive
As
Arsenic
AsB
Arsenobetaine
DMA
Dimethylarsinate
iAsIII
Arsenite
iAs
Arsenate
MMA
Monomethylarsonate
tAs
Total arsenic
uAs
Unknown arsenic
UC
Ulcerative Colitis
TCM
Traditional Chinese Medicine
OTU
Operational Taxonomic Unit
LEfSe
Linear Discriminant Analysis Effect Size
R2
Coefficient of Determination
LDA
Linear Discriminant Analysis
LOD
Limit of Detection
LOQ
Limit of Quantification
CRM
Certified Reference Materials
OPLS-DA
Orthogonal Partial Least Squares Discriminant Analysis
VIP
Variable Importance in the Projection
RSD
Relative Standard Deviations
Cef
Ceftriaxone
F/B
Firmicutes/Bacteroidota
PMI
Primary Methylation Index
SMI
Secondary Methylation Index
TMI
Total Methylation Index
CA
Cholic Acid
DCA
Deoxycholic Acid
CDCA
Chenodeoxycholic Acid
HDCA
Hyodeoxycholic Acid
LCA
Lithocholic acid
UDCA
Ursodeoxycholic Acid
GCA
Glycocholic Acid
GCDCA
Glycochenodeoxycholic Acid
TCA
Taurocholic Acid
α-MCA
Alpha-Muricholic Acid
β-MCA
Beta-Muricholic Acid
TCDCA
Taurochenodeoxycholic Acid
TUDCA
Tauroursodeoxycholic Acid
TDCA
Taurodeoxycholic Acid
GUDCA
Glycoursodeoxycholic Acid
T-α-MCA
Tauro-Alpha-Muricholic acid
GCDCA-d4
[2H4]-Glycochenodeoxycholic Acid
GSH
Glutathione
SOD
Superoxide Dismutase
MDA
Malondialdehyde
8-OHdG
8-Hydroxydeoxyguanosine

Data availability

No data was used for the research described in the article.

Cited by (0)

1

Linkang Chen and Chengji Li are co-first authors.