# Differential Proteomic Analysis of Low-Dose Chronic Paralytic Shellfish Poisoning

**Authors:** Xiujie Liu, Fuli Wang, Huilan Yu, Changcai Liu, Junmei Xia, Yangde Ma, Bo Chen, Shilei Liu

PMC · DOI: 10.3390/md22030108 · Marine Drugs · 2024-02-26

## TL;DR

This study uses proteomic analysis to explore brain protein changes in mice with chronic low-dose shellfish poisoning, revealing potential impacts on synaptic and nervous system functions.

## Contribution

The study introduces a novel low-dose chronic model to investigate proteomic changes in the brain caused by shellfish poisoning.

## Key findings

- 6798 proteins were identified, with 123 showing significant changes due to shellfish poisoning.
- Proteins related to synaptic transmission and nervous system development were altered, indicating potential nerve damage.
- Key enzymes involved in ion transport and transferase activity were affected in the poisoned mice.

## Abstract

Shellfish poisoning is a common food poisoning. To comprehensively characterize proteome changes in the whole brain due to shellfish poisoning, Tandem mass tag (TMT)-based differential proteomic analysis was performed with a low-dose chronic shellfish poisoning model in mice. A total of 6798 proteins were confidently identified, among which 123 proteins showed significant changes (fold changes of >1.2 or <0.83, p < 0.05). In positive regulation of synaptic transmission, proteins assigned to a presynaptic membrane (e.g., Grik2) and synaptic transmission (e.g., Fmr1) changed. In addition, altered proteins in nervous system development were observed, suggesting that mice suffered nerve damage due to the nervous system being activated. Ion transport in model mice was demonstrated by a decrease in key enzymes (e.g., Kcnj11) in voltage-gated ion channel activity and solute carrier family (e.g., Slc38a3). Meanwhile, alterations in transferase activity proteins were observed. In conclusion, these modifications observed in brain proteins between the model and control mice provide valuable insights into understanding the functional mechanisms underlying shellfish poisoning.

## Linked entities

- **Genes:** GRIK2 (glutamate ionotropic receptor kainate type subunit 2) [NCBI Gene 2898], FMR1 (fragile X messenger ribonucleoprotein 1) [NCBI Gene 2332], KCNJ11 (potassium inwardly rectifying channel subfamily J member 11) [NCBI Gene 3767], SLC38A3 (solute carrier family 38 member 3) [NCBI Gene 10991]
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** SLC38A3 (solute carrier family 38 member 3) [NCBI Gene 10991] {aka DEE102, G17, NAT1, SN1, SNAT3}, FMR1 (fragile X messenger ribonucleoprotein 1) [NCBI Gene 2332] {aka FMRP, FRAXA, POF, POF1}, KCNJ11 (potassium inwardly rectifying channel subfamily J member 11) [NCBI Gene 3767] {aka BIR, HHF2, IKATP, KIR6.2, MODY13, PHHI}, GRIK2 (glutamate ionotropic receptor kainate type subunit 2) [NCBI Gene 2898] {aka EAA4, GLR6, GLUK6, GLUR6, GluK2, MRT6}
- **Diseases:** nerve damage (MESH:D000080902), food poisoning (MESH:D005517), Paralytic (MESH:D000092164), Shellfish Poisoning (MESH:D057096)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC10972186/full.md

## References

25 references — full list in the complete paper: https://tomesphere.com/paper/PMC10972186/full.md

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Source: https://tomesphere.com/paper/PMC10972186