Interactions of micronutrients can affect absorption and bioavailability of other nutrients by a number of mechanisms. In aqueous solutions, and at higher uptake levels, competition between elements with similar chemical characteristics and uptake process can take place. The consequences of these interactions may depend on the relative concentrations of the nutrients. In this work, we measure the effects of increasing concentrations of iron, zinc, and copper on iron and copper uptake in Caco-2 cells. Intracellular Fe or Cu levels were affected by incubating with increased concentrations of metals. However, when the cells already had different intracellular metal concentration, the uptake of Fe or Cu was nor affected. In competition studies, we showed that Cu and Zn inhibited Fe uptake, and while Fe inhibited Cu uptake, Zn did not. When the three metals were given together (1:1:1 ratio), Fe or Cu uptake was inhibited approximately 40%. These results point to a potential risk in the absorption and bioavailability of these minerals by the presence of other minerals in the diet. This aspect must be considered in food supplementation and fortification programs.

Background: Iron is necessary for neuronal function but in excess generates neurodegeneration. Although most of the components of the iron homeostasis machinery have been described in neurons, little is known about the particulars of their iron homeostasis. In this work we characterized the response of SH-SY5Y neuroblastoma cells and hippocampal neurons to a model of progressive iron accumulation. Results: We found that iron accumulation killed a large proportion of cells, but a sub-population became resistant to iron. The surviving cells evoked an adaptative response consisting of increased synthesis of the iron-storage protein ferritin and the iron export transporter IREG1, and decreased synthesis of the iron import transporter DMT1. Increased expression of IREG1 was further substantiated by immunocytochemistry and iron efflux experiments. IREG1 expression directly correlated with iron content in SH-SY5Y and hippocampal cells. Similarly, a high correlation was found between IREG1 expression and the rate of iron efflux from SH-SY5Y cells. Conclusions: Neuronal survival of iron accumulation associates with increased expression of the efflux transporter IREG1. Thus, the capacity of neurons to express IREG1 may be one of the clues to iron accumulation survival.

Obesity is characterized by mild chronic inflammation that linked with impaired iron homeostasis. Studies in human and murine show that there is a transgenerational epigenetic inheritance via the gametes in obesity, however, there is little information on changes in the expression of microRNAs related to inflammation and iron homeostasis in spermatozoa from obese subjects. The present study investigated the expression of microRNAs related to inflammation (miR-21 y miR-155) and iron nutrition (miR-122 and miR-200b) in plasma, peripheral blood mononuclear cells (PBMC) and spermatozoa from normozoospermic controls (Cn; n=17; BMI: 24,6±2,0) and obese (Ob; n=17; BMI: 32,6±4,4) men. To determine the inflammation levels we measured IL-6, TNFα and monocyte chemoattractant protein-1 (MCP1) by Magnetic Luminex® Assay. mRNA expression of IL6, TNFα and hepcidin (HAMP) in PBMC were evaluated by RT-qPCR. The analysis of microRNAs were performed using the Taqman® assays. The iron content in PBMC, seminal plasma and spermatozoa was determined by Inductively Coupled Plasma Mass Spectrometry (ICP-MS). High serum IL6, TNFα and MCP1 levels were observed in Ob group (p<0.05). Gene expression analysis shown an increased abundance relative of TNFα (p=0.018), HAMP (p=0.03) and IL6 (p=0.02) in PBMC from obese subjects. Also, we observed high levels of serum ferritin (p=0.03), iron content in seminal plasma (p=0.04) and spermatozoa (p=0.002), but lower serum Fe (p=0.007) in obese subjects. In the Ob group a high expression of miR-155 (p=0.02) and miR-21 (p=0.03) was observed in PBMC and miR-122 (p=0.03) in plasma. In sperm, both miR-155 (p=0.004) and miR-122 (p=0.028) were high in the Ob group. Our results showed that obese subjects have increased expressions of miR-155 and miR-122, two microRNAs that were previously related with inflammation and iron metabolism, respectively, at both the systemic and sperm levels.