Abstract

Maize is the predominant food source contaminated by fumonisins and this has particular health risks for communities consuming maize as a staple diet. The main biochemical effect of fumonisins is the inhibition of ceramide biosynthesis causing an increase in sphingoid bases and sphingoid base 1-phosphates and a depletion of the complex sphingolipids, thereby disrupting lipid metabolism and sphingolipid-mediated processes and signalling systems. Attempts to use the elevation of sphinganine as a human biomarker of fumonisin exposure have to date been unsuccessful. Consequently, recent research has focussed on developing a urinary exposure biomarker based on the measurement of the nonmetabolised toxin. In animals, fumonisins are poorly absorbed in the gut and are mostly excreted unmetabolised in faeces, with only a small percentage (0.25-2.0%) in urine. This appears to also be true in humans were fumonisin B1 (FB1) is detectable in urine soon after exposure, but in very small amounts relative to total intake. However, with modern sensitive and selective analytical methods such as liquid chromatography-tandem mass spectrometry, these low levels can be readily determined. The first study to show a positive correlation between consumption of maize and urinary FB1 was conducted in a Mexican population consuming tortillas as a staple food. Further validation of this relationship was achieved in a South African subsistence farming community with a positive correlation between urinary FB1 and fumonisin exposure, as assessed by food analysis and food intake data. The most recent developments are aimed at measuring multiple mycotoxin biomarkers in urine, including FB1. Current exposure studies in Guatemala are combining the urinary biomarker with measurement of sphinganine-1-phosphate in blood spots as a measure of biochemical effect. Thus, the urinary FB1 biomarker could contribute considerably in assessing the adverse health impact of fumonisin exposure.

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