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Updated: May 10, 2025

Quantification of Fungal Colonization, Sporogenesis, and Production of Mycotoxins Using Kernel Bioassays
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Exploring the cardiotoxic potential of fumonisin B1 through inflammatory pathways and epigenetic modifications: A

Selwyn Kyle Gounder1, Anil Amichund Chuturgoon1, Terisha Ghazi1

  • 1Discipline of Medical Biochemistry, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban, 4041, South Africa.

Toxicon : Official Journal of the International Society on Toxinology
|April 26, 2025
PubMed

Insights

Fumonisin B1 (FB1), a mycotoxin, harms heart health by disrupting sphingolipid metabolism and increasing inflammation. It also causes epigenetic changes that worsen cardiovascular disease, highlighting the need for further research.

Area of Science:

  • Toxicology
  • Cardiovascular Science
  • Epigenetics

Background:

  • Fumonisin B1 (FB1) is a mycotoxin from Fusarium fungi contaminating food, posing health risks.
  • Its specific role in causing and worsening cardiovascular disease requires further elucidation.
  • FB1 impacts sphingolipid metabolism, inflammation, and epigenetic regulation.

Purpose of the Study:

  • To review the cardiotoxic effects of FB1.
  • To explore FB1's impact on sphingolipid metabolism, inflammation, and epigenetics.
  • To highlight the need for research on FB1-related cardiotoxicity.

Main Methods:

  • Literature review of studies on FB1 and cardiotoxicity.
  • Analysis of FB1's effects on sphingolipid metabolism (ceramide synthase inhibition).
  • Examination of FB1's influence on inflammatory markers (IL-6, IL-1β) and epigenetic modifications (DNA methylation, histone modifications, microRNA expression).

Main Results:

  • FB1 inhibits ceramide synthase, disrupting sphingolipid metabolism and leading to cellular dysfunction.
  • FB1 increases pro-inflammatory cytokines, contributing to hypertension and heart failure.
  • FB1 induces epigenetic alterations, including DNA hypermethylation and altered histone marks, impacting gene expression and disease progression.

Conclusions:

  • FB1 exerts cardiotoxic effects through disruption of sphingolipid metabolism, inflammation, and epigenetic changes.
  • These mechanisms contribute to hypertension, heart failure, and cardiovascular disease progression.
  • Further research is crucial to understand the intricate links between FB1, inflammation, epigenetics, and cardiotoxicity for better risk management.
Keywords:
CardiotoxicityDNA methylationFumonisin B1Histone modificationInflammationmicroRNA

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