Document Detail


Deoxynivalenol: mechanisms of action, human exposure, and toxicological relevance.
MedLine Citation:
PMID:  20798930     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The trichothecene mycotoxin deoxynivalenol (DON) is produced in wheat, barley and corn following infestation by the fungus Fusarium in the field and during storage. Colloquially known as "vomitoxin" because of its emetic effects in pigs, DON has been associated with human gastroenteritis. Since DON is commonly detected in cereal foods, there are significant questions regarding the risks of acute poisoning and chronic effects posed to persons ingesting this trichothecene. A further challenge is how to best manage perceived risks without rendering critical food staples unavailable to an ever-expanding world population. In experimental animal models, acute DON poisoning causes emesis, whereas chronic low-dose exposure elicits anorexia, growth retardation, immunotoxicity as well as impaired reproduction and development resulting from maternal toxicity. Pathophysiologic effects associated with DON include altered neuroendocrine signaling, proinflammatory gene induction, disruption of the growth hormone axis, and altered gut integrity. At the cellular level, DON induces ribotoxic stress thereby disrupting macromolecule synthesis, cell signaling, differentiation, proliferation, and death. There is a need to better understand the mechanistic linkages between these early dose-dependent molecular effects and relevant pathological sequelae. Epidemiological studies are needed to determine if relationships exist between consumption of high DON levels and incidence of both gastroenteritis and potential chronic diseases. From the perspective of human health translation, a particularly exciting development is the availability of biomarkers of exposure (e.g. DON glucuronide) and effect (e.g. IGF1) now make it possible to study the relationship between DON consumption and growth retardation in susceptible human populations such as children and vegetarians. Ultimately, a fusion of basic and translational research is needed to validate or refine existing risk assessments and regulatory standards for this common mycotoxin.
Authors:
James J Pestka
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review     Date:  2010-08-27
Journal Detail:
Title:  Archives of toxicology     Volume:  84     ISSN:  1432-0738     ISO Abbreviation:  Arch. Toxicol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-02     Completed Date:  2010-12-02     Revised Date:  2014-09-15    
Medline Journal Info:
Nlm Unique ID:  0417615     Medline TA:  Arch Toxicol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  663-79     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cereals / metabolism,  microbiology
Disease Models, Animal*
Environmental Exposure
Food Microbiology
Fusarium / metabolism*
Gastroenteritis / microbiology
Gastrointestinal Tract / physiopathology
Humans
Male
Mice
Ribosomes / metabolism
Risk Assessment
Signal Transduction
Swine
Translational Medical Research
Trichothecenes / metabolism,  toxicity*
Grant Support
ID/Acronym/Agency:
ES 3358/ES/NIEHS NIH HHS; R01 ES003358/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Trichothecenes; 51481-10-8/deoxynivalenol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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