SPHINGOSINE-RELATED MYCOTOXINS IN PLANT AND ANIMAL DISEASES

Citation
Dg. Gilchrist et al., SPHINGOSINE-RELATED MYCOTOXINS IN PLANT AND ANIMAL DISEASES, Canadian journal of botany, 73, 1995, pp. 459-467
Citations number
57
Journal title
ISSN journal
00084026
Volume
73
Year of publication
1995
Supplement
1
Pages
459 - 467
Database
ISI
SICI code
0008-4026(1995)73:<459:SMIPAA>2.0.ZU;2-E
Abstract
The AAL-toxins and fumonisins are a group of chemically related phytot oxic congeners produced by Alternaria alternata f. sp. lycopersici and Fusarium moniliforme, respectively, that also are widespread mycotoxi ns with important health implications. These mycotoxins, which bear a structural relationship to the sphingoid base, sphingosine, also incit e maladies in animals ranging from neoplasms to renal, neural, and hep atic necrosis. A. alternata f. sp. lycopersici causes the Alternaria s tem canker disease in tomatoes, while F. moniliforme causes pink ear r ot of maize and is associated with post-harvest contamination of many different food staples. These toxins are potent inhibitors of ceramide synthase in plants and animals. Sphingoid bases are mediators of sign al transduction leading to neoplasms and necrosis in animals. Signific ant inhibition of ceramide synthase in microsomal preparations of toma to occurs at 20 nM with an I-50 in the range of 35-40 nM for both AAL- toxin, TA, and fumonisin, FB1. In plants, specific alterations of phys iological processes associated with cellular response to these toxins appears to be required for cell death. A net decrease in sucrose influ x to treated leaves occurs within 4 h of AAL-toxin treatment. Untreate d leaves of toxin-resistant and sensitive isolines of tomato show sign ificant differences in sucrose transport capacity. Exogenous applicati on of sucrose transport inhibitors mimicked AAL-toxin symptoms and enh anced cell death in susceptible lines of tomato. Conversely, the accum ulation of the ethylene precursor 1-aminocyclopropane-1-carboxylic aci d (ACC) occurred in 1 h and increased rapidly during the next 6 h afte r exposure to AAL-toxin. ACC accumulation is followed by a burst in et hylene within 12 h. Application of specific inhibitors of ethylene syn thesis or ethylene action results in a decrease in toxin-induced cell death. These toxins appear to be useful tools for defining biochemical and molecular features common to induced cell death in both plants an d animals.