Fumonisins are a family of potentially carcinogenic mycotoxins produced by Fusarium verticillioides. Several fumonisins have been identified with fumonisin B1 (FB1 ) being the most toxic. The canonical mechanism of FB1 toxicity is centered on its structural resemblance with sphinganine and consequent competitive inhibition of ceramide synthase and disruption of lipidomic profiles. Recent and emerging evidence at the molecular level has identified the disruption of mitochondria and excessive generation of toxic reactive oxygen species (ROS) as alternative/additional mechanisms of toxicity. The understanding of how these pathways contribute to FB1 toxicity can lead to the identification of novel, effective approaches to protecting vulnerable populations. Natural compounds with antioxidant properties seem to protect against the induced toxic effects of FB1 . Rooibos (Aspalathus linearis), endemic to South Africa, has traditionally been used as a medicinal herbal tea with strong scientific evidence supporting its anecdotal claims. The unique composition of phytochemicals and combination of metabolic activators, adaptogens and antioxidants make rooibos an attractive yet underappreciated intervention for FB1 toxicoses. In the search for a means to address FB1 toxicoses as a food safety problem in developing countries, phytomedicine and traditional knowledge systems must play an integral part. This review aims to summarize the growing body of evidence succinctly, which highlights mitochondrial dysfunction as a secondary toxic effect responsible for the FB1 -induced generation of ROS. We further propose the potential of rooibos to combat this induced toxicity based on its integrated bioactive properties, as a socio-economically viable strategy to prevent and/or repair cellular damage caused by FB1 .
Keywords: fumonisin B1; mitochondria; oxidative stress; phytomedicine; rooibos.
© 2020 John Wiley & Sons, Ltd.