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Deoxynivalenol: signaling pathways and human exposure risk assessment--an update
- Source :
- Archives of toxicology. 88(11)
- Publication Year :
- 2014
-
Abstract
- Deoxynivalenol (DON) is a group B trichothecene and a common contaminant of crops worldwide. This toxin is known to cause a spectrum of diseases in animals and humans such as vomiting and gastroenteritis. Importantly, DON could inhibit the synthesis of protein and nucleonic acid and induce cell apoptosis in eukaryote cells. The transduction of signaling pathways is involved in the underlying mechanism of the cytotoxicity of DON. Mitogen-activated protein kinase and Janus kinase/signal transducer and activator of transcription seem to be two important signaling pathways and induce the inflammatory response by modulating the binding activates of specific transcription factors. This review mainly discussed the toxic mechanism of DON from the vantage point of signaling pathways and also assessed the profiles of DON and its metabolites in humans. Importantly, we conducted a human exposure risk assessment of DON from cereals, cereal-based foods, vegetables, water, and animal-derived foods in different countries. Some regular patterns of DON occurrence in these countries are suggested based on an analysis of global contamination with DON. This review should provide further insight for the toxic mechanism study of DON and human exposure risk assessment, thereby facilitating mycotoxin control strategies.
- Subjects :
- MAPK/ERK pathway
business.industry
Health, Toxicology and Mutagenesis
Trichothecene
JAK-STAT signaling pathway
Food Contamination
General Medicine
Environmental Exposure
Biology
Toxicology
Risk Assessment
Biotechnology
Immunology
STAT protein
Animals
Humans
Signal transduction
Janus kinase
Protein kinase A
business
Trichothecenes
Transcription factor
Environmental Monitoring
Signal Transduction
Subjects
Details
- ISSN :
- 14320738
- Volume :
- 88
- Issue :
- 11
- Database :
- OpenAIRE
- Journal :
- Archives of toxicology
- Accession number :
- edsair.doi.dedup.....761bae894282f20179dce19b54ad7efc