Studies on the toxicity of deoxynivalenol (DON), sodium metabisulfite, DON-sulfonate (DONS) and de-epoxy-DON for porcine peripheral blood mononuclear cells and the Intestinal Porcine Epithelial Cell lines IPEC-1 and IPEC-J2, and on effects of DON and DONS on piglets.

The in vitro effects of deoxynivalenol (DON), de-epoxy-DON, DON-sulfonate (DONS) and sodium metabisulfite (Na(2)S(2)O(5), SBS) on porcine peripheral blood mononuclear cells (PBMC), and on the Intestinal Porcine Epithelial Cell lines IPEC-1 and IPEC-J2 were examined by using the MTT assay. In addition, an uncontaminated and a DON contaminated triticale were included in diets either untreated (CON, FUS) or SBS treated (CON-SBS, FUS-SBS) and fed to piglets for 28 d starting from weaning. The diet concentrations of DON and DONS amounted to 0.156, 2.312, 0.084 and 0.275 mg and to<0.05, <0.05, <0.05 and 1.841 mg/kg, respectively. PBMC of the so-exposed piglets were also subjected to the MTT assay. Neither DONS and SBS nor de-epoxy-DON affected the viability of PBMC, IPEC-1 and IPEC-J2 significantly up to concentrations of 17, 8 and 23 microM, respectively. For DON, IC(50) values were estimated at 1.2+/-0.1, 1.3+/-0.5 and 3.0+/-0.8 microM for PBMC, IPEC-1 and IPEC-J2, respectively. PBMC from piglets fed the SBS treated diets were characterized by a significantly decreased stimulation index and an increased IgA supernatant concentration with the SBS effect being significantly more pronounced after feeding the FUS-SBS diet. Further studies should clarify the possible impact of SBS on the porcine immune system.

Differential control of isocitrate lyase gene transcription by non-fermentable carbon sources in the milk yeast Kluyveromyces lactis.

The KlICL1 gene, encoding isocitrate lyase in Kluyveromyces lactis, is essential for ethanol utilization. Deletion analyses identified two functional promoter elements, CSRE-A and CSRE-B. Transcription is activated on ethanol, but not on glucose, glycerol or lactate. Expression depends on the KlCat8p transcription factor and KlSip4p binds to the promoter elements. Glycerol diminishes KlICL1 expression and a single carbon source responsive element (CSRE) sequence is both necessary and sufficient to mediate this regulation. The glycerol effect is less pronounced in Saccharomyces cerevisiae than in K. lactis. Mutants lacking KlGUT2 (which encodes the glycerol 3-phosphate dehydrogenase) still show reduced expression in glycerol, whereas mutants deficient in glycerol kinase (Klgut1) do not. We conclude that a metabolite of glycerol is required for this regulation.