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Inhibition of sphingolipid biosynthesis by fumonisins. Implications for diseases associated with Fusarium moniliforme.
TLDR
Findings suggest that disruption of the de novo pathway of sphingolipid biosynthesis may be a critical event in the diseases that have been associated with consumption of fumonisins. Expand
Fumonisins disrupt sphingolipid metabolism, folate transport, and neural tube development in embryo culture and in vivo: a potential risk factor for human neural tube defects among populations
TLDR
It is proposed that fumonisins are potential risk factors for NTD, craniofacial anomalies, and other birth defects arising from neural crest cells because of their apparent interference with folate utilization. Expand
Sphingolipids--the enigmatic lipid class: biochemistry, physiology, and pathophysiology.
TLDR
Findings illustrate how an understanding of the function of sphingolipids can help solve questions in toxicology and this is undoubtedly only the beginning of this story. Expand
Sphingolipid metabolism: roles in signal transduction and disruption by fumonisins.
TLDR
All these processes--the effects of fumonisins on sphingolipid metabolism, the pathways altered by perturbation of sphingosine metabolism, and the complex cellular behaviors regulated by sphingoipids--must be borne in mind when evaluating the pathologic effects of FUMonisins. Expand
Fumonisin- and AAL-Toxin-Induced Disruption of Sphingolipid Metabolism with Accumulation of Free Sphingoid Bases
TLDR
In plants the disease symptoms associated with A. alternata and F. moniliforme infection may be due to disruption of sphingolipid metabolism, which suggests that the primary biochemical lesion is inhibition of de novo ceramide synthesis and reacylation of free sphingoid bases. Expand
Alteration of tissue and serum sphinganine to sphingosine ratio: an early biomarker of exposure to fumonisin-containing feeds in pigs.
TLDR
The results of this study show that free sphinganine is elevated in liver, lung, and kidney, from pigs consuming feeds containing fumonisin concentrations of 23 ppm or greater, and this supports the hypothesis that inhibition of sphingosine and sphingAnine N-acyltransferase plays an important role in the pathogenesis of animal diseases associated with consumption of feed containing fUMonisins. Expand
Sphingolipid perturbations as mechanisms for fumonisin carcinogenesis.
TLDR
The balance between the rates of apoptosis and proliferation is important in tumorigenesis, cells sensitive to the proliferative effect of decreased CER and increased sphingosine 1-phosphate may be selected to survive and proliferate when free sphingoid base concentration is not growth inhibitory. Expand
The kinetics of urinary fumonisin B1 excretion in humans consuming maize-based diets.
TLDR
The results support the use of urinary FB(1) to assess ongoing exposure in population-based studies and validate a method to isolate urinary FB on C(18) -SPE cartridges for international shipment. Expand
Dietary fumonisin B1 induces disruption of sphingolipid metabolism in Sprague-Dawley rats: a new mechanism of nephrotoxicity.
TLDR
Urine rather than serum is the fluid of choice for detecting elevated free sphingoid bases generated as a consequence of fumonisin-induced kidney damage. Expand
Transformation-mediated complementation of a FUM gene cluster deletion in Fusarium verticillioides restores both fumonisin production and pathogenicity on maize seedlings.
TLDR
The data indicate that fumonisin production may have been lost by deletion of the FUM cluster in the banana population of F. verticillioides but that it could be restored by molecular genetic complementation. Expand
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