低剂量麻痹性贝类毒素慢性中毒的差异蛋白质组学分析。

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

机构信息

State Key Laboratory of NBC Protection for Civilian, Beijing 102205, China.

出版信息

Mar Drugs. 2024 Feb 26;22(3):108. doi: 10.3390/md22030108.

DOI:10.3390/md22030108

PMID:38535448

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10972186/

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, < 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.

摘要

贝类中毒是一种常见的食物中毒。为了全面描述贝类中毒导致全脑蛋白质组变化，我们使用低剂量慢性贝类中毒模型在小鼠中进行了串联质量标签（TMT）差异蛋白质组分析。共鉴定出 6798 种蛋白质，其中 123 种蛋白质发生明显变化（倍数变化>1.2 或<0.83，<0.05）。在突触传递的正调节中，分配到突触前膜（例如，Grik2）和突触传递（例如，Fmr1）的蛋白质发生变化。此外，还观察到神经系统发育过程中改变的蛋白质，表明由于神经系统被激活，小鼠受到神经损伤。通过电压门控离子通道活性和溶质载体家族（例如，Slc38a3）中关键酶（例如，Kcnj11）的减少，在模型小鼠中证明了离子转运。同时，观察到转移酶活性蛋白的改变。总之，在模型和对照小鼠的脑组织蛋白之间观察到的这些修饰为理解贝类中毒的功能机制提供了有价值的见解。