Arsenic induced neurotoxicity in the brain of ducks: The potential involvement of the gut-brain axis

ElsevierVolume 81, January 2024, 127336Journal of Trace Elements in Medicine and BiologyAuthor links open overlay panel, , , , , , , , , , Highlights•

ATO exposure disrupted the diversity of gut microbiota.

ATO exposure induced inflammatory reaction in duodenum of duck.

Autophagy and apoptosis were involved in ATO-induced neurotoxicity.

Mechanism of gut-brain axis provided a novel insight into the arsenic toxicity.

AbstractBackground

Arsenic is a widely distributed ecotoxic pollutant that has been found to cause neurotoxicity in a variety of species. Gut-brain axis is a two-way information network between the gut microbiome and the brain, which is closely related to organismal health. However, the role of the gut-brain axis in arsenic-induced neurotoxicity remains largely unknown.

Methods

In order to explore whether there is a relationship between brain and gut microbiota of meat ducks, we performed molecular biological detection including RT-qPCR and Western blot, as well as morphological detection including, HE staining and immunohistochemistry. Meanwhile, intestinal contents were analyzed using 16 S ribosomal RNA gene sequencing and analysis

Results

In this study, we investigated whether arsenic trioxide (ATO) can activate the gut microbiome-brain axis to induce intestinal and brain injury. The results showed that ATO-exposure disrupted the diversity balance of intestinal microbiota and integrity and injured the intestinal structure. ATO-exposure also reduced the number of glycogen and goblet cells in the duodenum. In addition, exposure to ATO caused intestinal inflammatory injury by activating NF-κB signaling pathway and promoting the expression of its target genes. Meanwhile, the tight junction-related proteins (ZO-1, occludin) of gut and brain were reduced by ATO exposure. Furthermore, results also revealed that ATO-exposure induced brain injury, including neuronal cell vacuolization and reduced numbers of neuronal cells in the cortex and hippocampus. Remarkably, ATO-exposure also disrupted neurotransmitter levels. Additionally, our further molecular mechanism study revealed that ATO-exposure increased the expression of autophagy and apoptosis related mRNA and proteins levels in the brain tissues.

Conclusion

Altogether, these findings provide a new insight into that ATO-exposure induced intestinal injury and aggravated neurotoxicity via the gut-brain axis.

Keywords

Arsenic

Gut microbiota

Gut-brain axis

Neurotoxicity

Duck

View Abstract

© 2023 Published by Elsevier GmbH.

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