# 2-(Methylthio) Benzothiazole (MTBT) Induces Cardiovascular Toxicity in Zebrafish Larvae and Investigates Its Mechanism

## TL;DR

This study shows that MTBT causes heart and blood vessel problems in zebrafish larvae and explains how it works.

## Contribution

This is the first study to systematically reveal MTBT's cardiovascular toxicity and its underlying mechanism.

## Key findings

- MTBT reduces heart rate and causes pericardial edema and cardiac malformations in zebrafish larvae.
- MTBT activates the apoptotic pathway by upregulating PTGS2, leading to cardiovascular toxicity.
- MTBT causes vascular structural defects and impairs circulatory function in zebrafish.

## Abstract

In this study, using zebrafish as a model, we found that 2-(Methylthio) benzothiazole (MTBT) decreased heart rate, caused pericardial edema and cardiac malformations, and reduced circulatory function in zebrafish larvae, leading to multiple vascular structural abnormalities. Mechanistic studies showed that MTBT activates the apoptotic pathway by upregulating PTGS2 expression, which in turn mediates cardiovascular development and functional toxicity. This study is the first to systematically reveal the cardiovascular toxicity of MTBT, providing a scientific basis for its environmental safety evaluation and risk management.

2-(Methylthio) benzothiazole (MTBT) is widely used in the industrial and pharmaceutical fields, but limited research has been conducted on its aquatic toxicity. In this study, we established a zebrafish model to systematically evaluate its developmental and functional toxicity, focusing on the cardiovascular systems of larvae. The results showed that MTBT significantly reduced heart rate, caused pericardial edema and deformity, delayed cardiac maturation, decreased stroke volume and cardiac output, and led to vascular structural defects. Mechanistically, MTBT upregulated the expression of the core target PTGS2, activated the apoptotic pathway, and mediated cardiovascular toxicity. This study is the first to systematically confirm the cardiovascular toxicity of MTBT, supplementing its toxicological database and providing a scientific basis for the establishment of environmental safety thresholds and risk management.