Document Detail

Chemistry and biological activity of AAL toxins.
MedLine Citation:
PMID:  8850626     Owner:  NLM     Status:  MEDLINE    
AAL toxins and fumonisins comprise a family of highly reactive, chemically related mycotoxins that disrupt cellular homeostasis in both plant and animal tissues. Two critical issues to resolve are the detection of the entire family in food matricies and the mode of cellular disruption. Analysis of the entire set of chemical congeners in food matrices is difficult but has been achieved by a combination of different HPLC and mass spectrometry strategies. The mode of cellular disruption is unknown but likely involves changes associated with the inhibition of ceramide synthase in both plants and animals. Toxin treated cells exhibit morphological and biochemical changes characteristic of apoptosis. Further evaluation of the specific genetic and biochemical changes that occur during toxin-induced cell death may aid in understanding the mole of the action of these mycotoxins.
C K Winter; D G Gilchrist; M B Dickman; C Jones
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Advances in experimental medicine and biology     Volume:  392     ISSN:  0065-2598     ISO Abbreviation:  Adv. Exp. Med. Biol.     Publication Date:  1996  
Date Detail:
Created Date:  1996-12-11     Completed Date:  1996-12-11     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0121103     Medline TA:  Adv Exp Med Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  307-16     Citation Subset:  IM    
Department of Food Science and Technology, University of California, Davis 95616, USA.
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MeSH Terms
Alternaria* / metabolism
Amidohydrolases / antagonists & inhibitors
Cell Death
Enzyme Inhibitors
Molecular Structure
Mycotoxins / analysis,  chemistry*,  pharmacology*
Plant Diseases
Grant Support
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Mycotoxins; EC 3.5.-/Amidohydrolases; EC

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