Please use this identifier to cite or link to this item: http://hdl.handle.net/11189/6867
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dc.contributor.authorGelderblom, WCAen_US
dc.contributor.authorAbel, Sen_US
dc.contributor.authorSmuts, CMen_US
dc.contributor.authorMarnewick, JLen_US
dc.contributor.authorMarasas, WFOen_US
dc.contributor.authorLemmer, ERen_US
dc.contributor.authorRamljak, Den_US
dc.date.accessioned2019-02-05T10:30:50Z-
dc.date.available2019-02-05T10:30:50Z-
dc.date.issued2001-
dc.identifier.citationGelderblom, W. C., Abel, S., Smuts, C. M., Marnewick, J., Marasas, W. F., Lemmer, E. R., & Ramljak, D. (2001). Fumonisin-induced hepatocarcinogenesis: mechanisms related to cancer initiation and promotion. Environmental health perspectives, 109(Suppl 2):291-300en_US
dc.identifier.urihttp://hdl.handle.net/11189/6867-
dc.descriptionArticleen_US
dc.description.abstractWe review the hepatocarcinogenic effects of fungal cultures of Fusarium verticillioides(= Fusarium moniliforme) strain MRC 826 in male BD IX rats. Subsequent chemical analyses of the fumonisin B (FB) mycotoxin content in the culture material used and long-term carcinogenesis studies with purified FB1 provide information about dose-response effects, relevance of hepatotoxicity during FB1-induced carcinogenesis, and the existence of a no-effect threshold. Fumonisin intake levels of between 0.08 and 0.16 mg FB/100 g body weight (bw)/day over approximately 2 years produce liver cancer in male BD IX rats. Exposure levels < 0.08 mg FB/100 g bw/day fail to induce cancer, although mild toxic and preneoplastic lesions are induced. The nutritional status of the diets used in the long-term experiments was marginally deficient in lipotropes and vitamins and could have played an important modulating role in fumonisin-induced hepatocarcinogenesis. Short-term studies in a cancer initiation/promotion model in rat liver provided important information about the possible mechanisms involved during the initial stages of cancer development by this apparently nongenotoxic mycotoxin. These studies supported the findings of long-term investigations indicating that a cytotoxic/proliferative response is required for cancer induction and that a no-effect threshold exists for cancer induction. The mechanisms proposed for cancer induction are highlighted and include the possible role of oxidative damage during initiation and the disruption of lipid metabolism, integrity of cellular membranes, and altered growth-regulatory responses as important events during promotion.en_US
dc.language.isoenen_US
dc.publisherPublished with support from the National Institute of Environmental Health Sciences, National Institutes of Health, U.S. Department of Health and Human Servicesen_US
dc.relation.ispartofEnvironmental Health Perspectives, 2001, 109(2):291-300.en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/za/-
dc.subjecthepatocarcinogenic effectsen_US
dc.subjectfungal culturesen_US
dc.subjectFusarium verticillioidesen_US
dc.subjectFusarium moniliformeen_US
dc.subjectmale BD IX ratsen_US
dc.subjectmycotoxin contenten_US
dc.titleFumonisin-induced hepatocarcinogenesis: mechanisms related to cancer initiation and promotionen_US
dc.typeArticleen_US
dc.identifier.doi10.1289/ehp.01109s2291-
dc.identifier.pmid11359698-
Appears in Collections:HWSci - Journal Articles (DHET subsidised)
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