Metabolic pathways of T-2 toxin
Language English Country Netherlands Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
- MeSH
- Rumen metabolism microbiology MeSH
- Bacteria metabolism MeSH
- Biotransformation MeSH
- Fungi metabolism MeSH
- Hydrolysis MeSH
- Hydroxylation MeSH
- Oxidation-Reduction MeSH
- Soil Microbiology MeSH
- Plants metabolism MeSH
- Fresh Water microbiology MeSH
- T-2 Toxin metabolism MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- T-2 Toxin MeSH
Among the naturally-occurring trichothecenes found in food and feed, T-2 toxin is the most potent and toxic mycotoxin. After ingestion of T-2 toxin into the organism, it is processed and eliminated. Some metabolites of this trichothecene are equally toxic or slightly more toxic than T-2 itself, and therefore, the metabolic fate of T-2 toxin has been of great concern. The main reactions in trichothecene metabolism are hydrolysis, hydroxylation and deep oxidation. Typical metabolites of T-2 toxin in an organism are HT-2 toxin, T-2-triol, T-2-tetraol, 3'-hydroxy-T-2, and 3'-hydroxy-HT-2 toxin. There are significant differences in the metabolic pathways of T-2 toxin between ruminants and non-ruminants. Ruminants have been more resistant to the adverse effects of T-2 toxin due to microbial degradation within rumen microorganisms. Some plant species are resistant to T-2 toxin, while others are capable of its intake and metabolisation.
References provided by Crossref.org
Comparison of Biogenic Amines and Mycotoxins in Alfalfa and Red Clover Fodder Depending on Additives
Forage as a primary source of mycotoxins in animal diets
Changes in metallothionein level in rat hepatic tissue after administration of natural mouldy wheat
