Dose-dependent lipid peroxidation induction on ex vivo intestine tracts exposed to chyme samples from fumonisins contaminated corn samples

•Fumonisins induced lipid peroxidation after short intestinal exposure.•Digestion process influences the lipid peroxidation induced by fumonisins.•The peroxidation induction is related to fumonisins concentrations. Fumonisins (FBs), Fusarium mycotoxins common food contaminant, are a potent inducer o...

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Published inToxicology in vitro Vol. 29; no. 5; pp. 1140 - 1145
Main Authors Garbetta, A., Debellis, L., De Girolamo, A., Schena, R., Visconti, A., Minervini, F.
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.08.2015
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ISSN0887-2333
1879-3177
1879-3177
DOI10.1016/j.tiv.2015.04.018

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Summary:•Fumonisins induced lipid peroxidation after short intestinal exposure.•Digestion process influences the lipid peroxidation induced by fumonisins.•The peroxidation induction is related to fumonisins concentrations. Fumonisins (FBs), Fusarium mycotoxins common food contaminant, are a potent inducer of oxidative stress and lipid peroxidation in intestinal cells. In order to verify this toxic effect in intestine tract, the aim was to assess lipid peroxidation (as malondialdehyde MDA increased levels) on intestine rat samples exposed to chyme samples from in vitro digestion of FBs contaminated corn samples. Naturally (9.61±3.2μg/gr), artificially (726±94μg/gr) and spiked corn samples at EU permitted FBs levels were digested and added to luminal side of Ussing chamber for 120min. Fumonisins-free corn sample was used as control. The MDA increase was observed just in 83% of intestine samples exposed at EU FBs levels and the digestion process seems to reduce this incidence (50% of samples). Malondialdehyde levels were FBs dose- and subject-related and ranged from 0.07±0.01 to 3.59±0.6nmol/mg. Highest incidence and MDA % increment (I) were found when intestine tracts were exposed to chymes from artificially corn sample. The induction of lipid peroxidation induced by FBs could be due to interactions between FBs and intestinal membranes, with consequent modifications in membrane permeability and oxygen diffusion–concentration, as suggested by other authors.
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ISSN:0887-2333
1879-3177
1879-3177
DOI:10.1016/j.tiv.2015.04.018