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

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.