Molecular and epigenetic modes of Fumonisin B₁ mediated toxicity and carcinogenesis and detoxification strategies

Abstract

Fumonisin B₁ (FB₁) is a natural contaminant of agricultural commodities that has displayed a myriad of toxicities in animals. Moreover, it is known to be a hepatorenal carcinogen in rodents and may be associated with oesophageal and hepatocellular carcinomas in humans. The most well elucidated mode of FB₁-mediated toxicity is its disruption of sphingolipid metabolism; however, enhanced oxidative stress, endoplasmic reticulum stress, autophagy, and alterations in immune response may also play a role in its toxicity and carcinogenicity. Alterations to the host epigenome may impact on the toxic and carcinogenic response to FB₁. Seeing that the contamination of FB₁ in food poses a considerable risk to human and animal health, a great deal of research has focused on new methods to prevent and attenuate FB₁-induced toxic consequences. The focus of the present review is on the molecular and epigenetic interactions of FB₁ as well as recent research involving FB₁ detoxification.

Keywords:

• Fusarium
• mycotoxins
• fumonisin B₁
• toxicity
• oxidative stress
• ER stress
• immunotoxicity
• epigenetics
• mycotoxin detoxification

Acknowledgements

The authors gratefully acknowledge Dr. Pragalathan Naidoo, University of KwaZulu-Natal, South Africa, for critical proofreading of the manuscript. The authors note with appreciation the value of four sets of comments and critiques provided by reviewers selected by the Editor and anonymous to the authors.

Declaration of interest

The authors declare to have no conflict of interest. The authors acknowledge the National Research Foundation (NRF) of South Africa for funding this review. The review was conceptualized by the authors and represents an unbiased professional assessment of available literature. The conclusions drawn are exclusively those of the authors. None of the authors have appeared during the last 10 years in any regulatory or legal proceedings related to the contents of this paper. We thank the NRF (Grant number 120820).