Please use this identifier to cite or link to this item: http://hdl.handle.net/11189/8558
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dc.contributor.authorAbdul, Naeem Sheiken_US
dc.contributor.authorMarnewick, Jeanine Len_US
dc.date.accessioned2022-07-07T13:15:55Z-
dc.date.available2022-07-07T13:15:55Z-
dc.date.issued2020-
dc.identifier.citationAbdul, N.S. & Marnewick, J.L. 2020. Fumonisin B1-induced mitochondrial toxicity and hepatoprotective potential of rooibos: An update. Journal of applied Toxicology. 40(4): 1602–1613. [https://doi.org/10.1002/jat.4036]en_US
dc.identifier.issn1099-1263-
dc.identifier.urihttp://hdl.handle.net/11189/8558-
dc.description.abstractFumonisins 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 socioeconomically viable strategy to prevent and/or repair cellular damage caused by FB1.en_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Applied Toxicologyen_US
dc.subjectFumonisin B1en_US
dc.subjectmitochondriaen_US
dc.subjectphytomedicineen_US
dc.subjectoxidative stressen_US
dc.subjectrooibosen_US
dc.titleFumonisin B1-induced mitochondrial toxicity and hepatoprotective potential of rooibos: An updateen_US
dc.identifier.doihttps://doi.org/10.1002/jat.4036-
dc.typeArticleen_US
Appears in Collections:Appsc - Journal Articles (DHET subsidised)
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