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Toxic fungal metabolites in food
Abstract:
About 100 fungal metabolites may cause cancer, embryological defects, or other histopathological effects in mammals. They are produced by a wide variety of fungi. Few of these metabolites have significant acute toxicity. With the exception of aflatoxin B1 and sterigmatocystin, there is no conclusive evidence that any of them is carcinogenic. However, several of the compounds are mutagenic. Cytochalasin D and T-2 toxin are probably teratogenic. A wide variety of other histopathological effects have been shown. Liver damage has been most frequently reported. In almost all cases the molecular bases of these effects have not been extensively investigated. Although much is known about the routes by which some of the compounds are synthesized in vivo, nothing is known about control at the molecular level of these biosynthetic routes. Little is known about the biological degradation of these compounds or about the levels and incidences of them in food and animal feed. Future work in all these areas will depend on the further development of sensitive assay methods that are applicable to their measurement in food, in animal feed, and in animal tissues and body fluids and on the application of these methods to define exposure to these compounds in the diet.
Insights
Fungal metabolites can cause various health issues in mammals, including cancer and birth defects, though conclusive evidence for carcinogenicity is limited. Further research is needed to understand their molecular effects and dietary exposure.
Area of Science:
- Mycology
- Toxicology
- Mammalian Pathology
Background:
- Approximately 100 fungal metabolites pose risks to mammals, potentially causing cancer, embryological defects, and histopathological changes.
- While acute toxicity is generally low, some metabolites are mutagenic and potentially teratogenic, with liver damage being a common histopathological effect.
Purpose of the Study:
- To review the known and potential health effects of fungal metabolites in mammals.
- To highlight the gaps in knowledge regarding the molecular mechanisms, biosynthesis, degradation, and dietary occurrence of these compounds.
- To emphasize the need for advanced assay methods for accurate exposure assessment.
Main Methods:
- Literature review of fungal metabolites and their toxicological effects.
- Analysis of existing evidence on carcinogenicity, mutagenicity, and teratogenicity.
- Identification of research gaps in molecular mechanisms and exposure assessment.
Main Results:
- Limited conclusive evidence for carcinogenicity, except for aflatoxin B1 and sterigmatocystin.
- Several fungal metabolites are mutagenic; Cytochalasin D and T-2 toxin are likely teratogenic.
- Molecular bases for observed histopathological effects, especially liver damage, are largely uninvestigated.
Conclusions:
- Significant knowledge gaps exist regarding the molecular basis of fungal metabolite toxicity, their biosynthesis, and degradation pathways.
- Accurate measurement of dietary exposure requires the development and application of sensitive assay methods.
- Further research is crucial to fully understand and mitigate the risks associated with fungal metabolites in food and feed.