N-Acetyl-d-neuraminic acid (NANA), more commonly known by its trivial name sialic acid, is an endogenous human and ubiquitous nutritional monosaccharide. As a bound sugar at the terminal positions of glycans NANA is known to play important roles in many biological events. The data that exist on the occurrence of the free monosaccharide in breast milk and nutrition, however, are less commonly discussed. In most foods of animal origin, sialic acid occurs as a mixture of NANA and N-glycolyl-d-neuraminic acid (NGNA), a hydroxylated derivative of NANA that is not found in humans. The dietary intake of NGNA has been identified as a risk factor for long-term adverse health effects. Therefore, we present summaries on the biochemistry, metabolism, bioavailability, and the data on NANA and NGNA levels that occur in diverse foods. Finally, we discuss the emerging data demonstrating that free NANA is linked to positive nutritional effects including pronounced antioxidative properties. These data and the extremely high safety profile of NANA justify dietary enrichment at levels that correspond to the dietary intake of NANA in infants through breast milk.

No abstract

No abstract

Exposure to the environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), produces hydronephrosis in developing mice, the etiology of which involves hyperplasia within the ureteric luminal epithelium. Dysregulation of epidermal growth factor receptor (EGFR), EGF, and transforming growth factor-alpha expression has been implicated as playing a role in TCDD-induced hydronephrosis. In this study, changes in the expression of genes encoding the EGFR and its cognate ligands in response to TCDD were evaluated within the developing ureter. C57BL/6 dams were injected ip with 30 mug/kg TCDD on gestational day (GD) 13 or 16 and fetal tissues removed on GD 17. Aryl hydrocarbon receptor (AHR) and AHR nuclear translocator messenger RNA (mRNA) were expressed in control and treated fetal tissues at GD 14 and 17. Prototypical AHR target genes, Cyp1a1, Cyp1a2, and Cyp1b1 were upregulated in TCDD-exposed fetal tissues, demonstrating AHR transcriptional activity at these developmental stages. Amphiregulin (AREG) and epiregulin, ligands for the EGFR, were induced at the transcriptional level in ureters of fetuses exposed to TCDD for 24 h. AREG mRNA was also induced by TCDD dose- and time-dependently in the mouse hepatoma cell line Hepa-1c1c7 (Hepa-1), mimicking the induction patterns of CYP1A1 mRNA. Other AHR ligands also induced AREG mRNA in Hepa-1 cells. Furthermore, variant Hepa-1 cells (TAOBP(r)c1 cells) virtually deficient in the AHR failed to display an increase in AREG mRNA in response to TCDD. Taken together, these data suggest that the AHR cross talks with the EGFR signaling pathway by directly inducing the expression of growth factors that are important for EGFR signaling in the developing mouse ureter.