Particulate matter induces arrhythmia-like cardiotoxicity in zebrafish embryos by altering the expression levels of cardiac development- and ion channel-related genes

Ecotoxicol Environ Saf. 2023 Sep 15:263:115201. doi: 10.1016/j.ecoenv.2023.115201. Epub 2023 Jul 5.

Abstract

Air pollution is a risk factor that increases cardiovascular morbidity and mortality. In this study, we investigated the cardiotoxicity of particulate matter (PM) exposure using a zebrafish embryo model. We found that PM exposure induced cardiotoxicity, such as arrhythmia, during cardiac development. PM exposure caused cardiotoxicity by altering the expression levels of cardiac development (T-box transcription factor 20, natriuretic peptide A, and GATA-binding protein 4)- and ion-channel (scn5lab, kcnq1, kcnh2a/b, and kcnh6a/b)-related genes. In conclusion, this study showed that PM induces the aberrant expression of cardiac development- and ion channel-related genes, leading to arrhythmia-like cardiotoxicity in zebrafish embryos. Our study provides a foundation for further research on the molecular and genetic mechanisms of cardiotoxicity induced by PM exposure.

Keywords: Arrhythmia; Heart; Heavy metal; Ion channel; Particulate matter; Zebrafish.

MeSH terms

  • Animals
  • Arrhythmias, Cardiac / chemically induced
  • Arrhythmias, Cardiac / genetics
  • Arrhythmias, Cardiac / metabolism
  • Cardiotoxicity* / genetics
  • Cardiotoxicity* / metabolism
  • Embryo, Nonmammalian / metabolism
  • Heart
  • Ion Channels / genetics
  • Particulate Matter / metabolism
  • Particulate Matter / toxicity
  • Zebrafish* / metabolism

Substances

  • Particulate Matter
  • Ion Channels