Oxidative metabolism in the cardiorespiratory system after an acute exposure to nickel-doped nanoparticles in mice.

There is an increasing concern over the harmful effects that metallic nanoparticles (NP) may produce on human health. Due to their redox properties, nickel (Ni) and Ni-containing NP are particularly relevant. Hence, the aim of this study was to establish the toxicological mechanisms in the cardiorespiratory oxidative metabolism initiated by an acute exposure to Ni-doped-NP. Mice were intranasally instilled with silica NP containing Ni (II) (Ni-NP) (1 mg Ni (II)/kg body weight) or empty NP as control, and 1 h after exposure lung, plasma, and heart samples were obtained to assess the redox metabolism. Results showed that, NP were mainly retained in the lungs triggering a significantly increased tissue O2 consumption rate, leading to Ni-NP-increased reactive oxygen species production by NOX activity, and mitochondrial H2O2 production rate. In addition, an oxidant redox status due to an altered antioxidant system showed by lung GSH/GSSG ratio decreased, and SOD activity increased, resulting in an increased phospholipid oxidation. Activation of circulating polymorphonuclear leukocytes, along with GSH/GSSG ratio decreased, and phospholipid oxidation were found in the Ni-NP-group plasma samples. Consequently, in distant organs such as heart, Ni-NP inhalation alters the tissue redox status. Our results showed that the O2 metabolism analysis is a critical area of study following Ni-NP inhalation. Therefore, this work provides novel data linking the redox metabolisms alterations elicited by exposure to Ni (II) adsorbed to NP and cardiorespiratory toxicity.

Alterations in oxygen metabolism are associated to lung toxicity triggered by silver nanoparticles exposure.

Along with the AgNP applications development, the concern about their possible toxicity has increasingly gained attention. As the respiratory system is one of the main exposure routes, the aim of this study was to evaluate the harmful effects developed in the lung after an acute AgNP exposure. In vivo studies using Balb/c mice intranasally instilled with 0.1 mg AgNP/kg b.w, were performed. 99mTc-AgNP showed the lung as the main organ of deposition, where, in turn, AgNP may exert barrier injury observed by increased protein content and total cell count in BAL samples. In vivo acute exposure showed altered lung tissue O2 consumption due to increased mitochondrial active respiration and NOX activity. Both O2 consumption processes release ROS triggering the antioxidant system as observed by the increased SOD, catalase and GPx activities and a decreased GSH/GSSG ratio. In addition, increased protein oxidation was observed after AgNP exposure. In A549 cells, exposure to 2.5 µg/mL AgNP during 1 h resulted in augment NOX activity, decreased mitochondrial ATP associated respiration and higher H2O2 production rate. Lung 3D tissue model showed AgNP-initiated barrier alterations as TEER values decreased and morphological alterations. Taken together, these results show that AgNP exposure alters O2 metabolism leading to alterations in oxygen metabolism lung toxicity. AgNP-triggered oxidative damage may be responsible for the impaired lung function observed due to alveolar epithelial injury.

Bioavailability studies of stabilized iron (II) sulfate by means of the prophylactic-preventive method.

The bioavailability of stabilized ferrous sulfate was studied by means of the prophylactic-preventive test in rats. For comparative purposes, ferrous sulfate was used as reference standard. The test was performed in male weaned rats during 3 weeks, which were randomized into three groups of ten animals each. A control group received a basal diet of low iron content while the other groups received the same diet added with iron at a dose of 15 mg/kg as FeSO4 7H2O and stabilized ferrous sulfate, respectively. Individual hemoglobin concentrations and weights were determined at the beginning and at the end of the study, and food intake was daily registered. Iron bioavailability (BioFe) of each source was calculated as the ratio between the amount of iron incorporated into hemoglobin during the treatment and the total iron intake per animal. A relative biological value was obtained as the ratio between the BioFe of stabilized ferrous sulfate and the reference standard given a value of 96%. Stabilized ferrous sulfate showed a high bioavailability, and when it is used to fortify dairy products as cheese and fluid milk in a dose of 15-20 mg of iron per kilogram, it behaved inertly in relation to the sensorial properties of the fortified food. These results suggest that this iron compound is a promising source to be use in food fortification.

[Causes and consequences of iron deficiency on human health]. / Causas y consecuencias de la deficiencia de hierro sobre la salud humana.

Anaemia and nutritional iron deficiency significantly affect the world population. In this article we discuss the main causes and consequences that this nutritional deficiency produces on human health.

[Iron metabolism: current concepts of an essential micronutrient]. / Metabolismo del hierro: conceptos actuales sobre un micronutriente esencial.

Iron is an essential micronutrient involved in multiple biochemical and physiological process. In this review we discuss the most relevant aspect of its metabolism in order to reach a better comprehension of the relevant roll that this micronutrient plays in human health.

Current knowledge of iron metabolism.

Iron plays many roles in human physiology. In this article, we summarize the basic and current knowledge of this essential micronutrient on human metabolism.

Zinc and iron interactions evaluated between different mineral sources in different nutritional matrixes.

We compared the absorption of BioZn, SFE-171, SO4Fe (reference standard) and SO4Zn (reference standard) alone or in combination in water and in an infant dessert. When mineral interactions were evaluated, zinc and iron were administered in a 1:1 molar relation. There 160 rats divided in 16 groups of 10 animals each which received: SO(4)65Zn, Bio65Zn, SO(4)65Zn + SO4Fe, Bio65Zn + SFE-171, SO(4)59Fe, 59SFE-171, SO(4)59Fe + SO4Zn and 59SFE-171 + BioZn either in water or an infant dessert. The results showed that BioZn has bioavailability similar to SO4Zn both in water (23.36 +/- 3.14% vs. 21.48 +/- 6.03%. respectively) and in an infant dessert (19.89 +/- 3.27% vs. 18.31 +/- 4.76%, respectively). When these zinc compounds were administered with iron no statistical difference of zinc absorption was found (Bio65Zn + SFE-171 in water 22.70 +/- 6.30%, Bio65Zn + SFE-171 in the infant dessert 18.07 +/- 5.89%, SO(4)65Zn + SO4Fe in water 24.67 +/- 5.70% and SO(4)65Zn + SO4Fe in the infant desert 20.56 +/- 5.20%). For iron, the absorption of 59SFE-171 in water was higher (p < .01) than SO(4)59Fe in water and 59SFE-171 + BioZn in water (32.35 +/- 8.32% vs. 26.27 +/- 8.83% vs. 23.69 +/- 8.37%, respectively). Iron absorption from SO(4)59Fe in water was higher (p < .01) than SO(4)59Fe + SO4Zn in water (26.27 +/- 8.83% vs. 20.21 +/- 8.72%, respectively). Iron absorption in the infant dessert was higher (p < .01) for 59SFE-171 + BioZn than SO(4)59Fe, 59SFE-171 and SO(4)59Fe + SO4Zn (22.81 +/- 6.97% vs. 16.12 +/- 6.14% vs. 16.90 +/- 6.23% vs. 15.04 +/- 6.25%, respectively). Statistical differences (p < .01) were found between iron absorption from 59SFE-171 in water and the infant dessert (32.35 +/- 8.32% vs. 16.90 +/- 6.23%, respectively) and for SO(4)59Fe (26.27 +/- 8.83% vs. 16.12 +/- 6.14% respectively). Zinc and iron interactions evaluated in a 1:1 molar relation of the minerals were observed only for iron absorption in water but not in infant dessert. No negative effect was found for zinc absorption neither in water nor in infant dessert.