Iron deficiency is the primary nutritional deficiency globally and iron dextran nanoparticles (IDN) are used for supplementation. Here we have applied theoretical, computational and experimental studies to understand the behavior of IDN and its interaction with a micrometric crosslinked gelatin scaffold (MCGS) to potentially develop a drug delivery system. Modeling single IDN reveals a complex network of interactions ranging from strong coordination bonds to weak van der Waals forces. Computational analyses reveal that multiple IDN (4 units) exhibit self-aggregation from 100 ns. In the presence of collagen (used to simulate MCGS), disaggregation occurs. The IDN-MCGS interactions are preferentially established (16-18 %) with the smaller/flexible amino acids alanine, proline and glycine. We hypothesize that the disaggregation of IDN in the presence of collagen is responsible for the low encapsulation efficiency (6.2-8.3 %) and low loading charge (1.9-3.7 %) during experimental encapsulation in MCGS (14-21 μm). X-ray diffraction reveal the absence of new crystalline arrangements resulting from the IDN-MCGS formulation. This is the first time that theoretical, computational and experimental studies were applied to IDN, multiple IDN and interactions with MCGS. These tools could be used for other protein scaffolds to predict drug encapsulation and delivery.

Iron dextran complex is commonly used to treat iron deficiency anemia (IDA). In this work, dextran was degraded and oxidized by UV/H2O2 treatment, and the product Dex-90 was chelated with FeCl3 to prepare the iron dextran complex (Dex-90-Fe). Results showed that UV/H2O2 treatment could significantly decrease the molecular weight of dextran and increase its carboxyl content, making it easier to chelate with iron (III). Moreover, Dex-90-Fe had a high iron content (30.77 % ± 0.87 %) and good thermal stability, which might be formed by Dex-90 with iron (III) via FeO bond. Furthermore, the therapeutic effects of Dex-90-Fe on IDA were investigated in rats. After oral administration, Dex-90-Fe significantly improved hematological parameters, increased serum iron and serum ferritin, facilitated iron accumulation in the liver and spleen, and regulated the gene expressions of iron homeostasis. In summary, the iron dextran complex Dex-90-Fe prepared from UV/H2O2-degraded dextran could be developed as an iron supplement.

Background/Objectives: Although essential for oxygen transport and DNA synthesis, excess iron is toxic and can damage organs such as the kidneys. Research has shown that iron overload induces kidney injury, and aging contributes to kidney dysfunction through functional and structural changes. The interaction between iron overload and aging remains poorly understood. Therefore, this study investigated their combined effects on renal microstructure and function using an iron-dextran-injected mouse model. Methods: Young and old mice were divided into control and iron overload groups, renal function was evaluated by serum creatinine and albuminuria, and urinary iron excretion was also measured to assess iron handling. The structural changes were assessed using histological analysis and electron microscopy. Results: Although the iron overload groups had similar blood iron levels, the old iron overload group exhibited significantly higher levels of albuminuria, urinary iron excretion, and serum creatinine compared with the young group. In the iron overload model, histological and ultrastructural analyses demonstrated iron accumulation in mesangial and endothelial cells, glomerular basement membrane thickening, and foot process widening, which were more pronounced in aged mice, suggesting that aging exacerbates iron-induced kidney injury. Conclusions: These findings demonstrate that aging increases susceptibility to iron-induced kidney injury, as shown by the accelerated glomerular injury observed in iron-overloaded aged mice. Therefore, elucidating the effects of aging on iron metabolism may contribute to identifying approaches for reducing age-associated renal injury.

This study aimed to evaluate the effectiveness of ferric carboxymaltose injection in the prevention of anaemia in suckling piglets. In group A (n = 8), piglets were administered iron in the form of iron carboxymaltose complex (Ferinject[®]) at a dose of 200 mg i.m. (neck muscle) at the age of 3 days. In group B (n = 8), piglets were given iron in the form of iron dextran (Ferribion[®]) at a dose of 200 mg i.m. (neck muscle) at the age of 3 days. In group C (n = 8, anaemic control group), iron was not administered until the age of 10 days. During the study, no statistically significant differences were observed in the parameters of red blood cell count or blood plasma iron concentration between the group that received iron carboxymaltase and the group that received iron dextran. The results of haematological and biochemical examinations achieved in our study show that the application of iron carboxymaltase was successful in preventing iron deficiency anaemia in piglets. The results indicate comparable efficacy of iron carboxymaltase and iron dextran.

Although iron is a vital component in the body, excessive iron leads to iron toxicity, which affects vital organs. In particular, the liver is considerably affected by iron toxicity because it stores the highest amount of iron in the body. Nonetheless, the relationship between iron overload and aging in the liver has not yet been clearly identified. This study aimed to observe the effects of aging on iron overload in the liver. Female C57BL/6J mice were randomly divided into vehicle control and iron overload groups (n = 7-22 per group). The iron overload group was injected with iron-dextran (Fe-dextran, ferric hydroxide dextran complex) (0.5 g/kg) for 4 weeks. After the experimental period, liver and blood samples were obtained from 2-, 15-, and 22-month-old mice. Liver weight, iron deposition, structural changes, cell death, extracellular matrix deposition, and fenestration of sinusoidal vessels were analyzed and compared between the groups. Additionally, biochemical analyses (aspartate aminotransferase, alanine aminotransferase, and serum total iron levels) were performed. The iron overload group exhibited significant differences compared with the control group with age. In the elderly iron overload model, iron deposition, inflammatory cell infiltration, and cell death were significantly increased (p < 0.0001). Moreover, deposition of the extracellular matrix and defenestration of sinusoidal fenestrae were observed among 22-month-old mice in the iron overload group. These results suggest that aging is a risk factor for iron-induced liver injury. Therefore, caution should be exercised when performing iron-related treatments in the elderly.

Anemia in pediatrics is often associated with chronic conditions such as chronic kidney disease (CKD). It can worsen the disease prognosis and affect quality of life. Injectable dosage forms are predominantly used in its treatment with various side effects. This randomized and parallel clinical trial aimed to compare the effectiveness of oral lactoferrin with intravenous (IV) iron dextran in managing anemia resulted from CKD in pediatrics. The study involved 60 children diagnosed with CKD-related anemia who were allocated into two separate groups. Group 1 consisted of 30 pediatric patients who received 100 mg of oral lactoferrin daily for a period of 3 months. Group 2 included 30 pediatric patients who were given IV iron dextran at a dosage of 50 mg three times weekly for 3 months. Both treatments are effective in treating CKD-induced anemia in pediatrics; however, oral lactoferrin demonstrated superior efficacy as there was a significant change within that group in levels of Hb, RBCs, MCH, iron, RDW-SD, MCHC, IL-6, and GDF-15 before and after treatment. In contrast, IV iron dextran showed significant changes within its group in iron, GFR, IL-6, GDF-15, and RDW-SD. After 3 months of treatment, no significant differences were observed between the two groups.

Iron overload in transfusion-dependent thalassemia patients represents a significant public health challenge due to its high mortality rate and risks of severe complications. Therefore, developing safe and effective therapeutic modalities for managing iron overload is critical, as current animal models inadequately replicate human conditions. The aim of this study was to investigate the effects of intravenous iron dextran on hepatocyte morphology, liver iron concentration, and serum iron profile changes as a model for hemochromatosis. An experimental design with a post-test-only control group method was conducted using animal models. Fifty rats were used and divided into ten groups, nine received different intravenous doses of iron dextran: 10, 20, 30, 40, 50, 60, 80, 100, and 120 mg/kg body weight (BW) and a control group received no treatment. The results showed that intravenous iron dextran starting at a dose of 10 mg/kg BW caused significant changes in liver iron concentration while starting at 20 mg/kg BW significantly affected hepatocyte morphology, transferrin levels, unsaturated iron binding capacity, serum iron levels, and transferrin saturation. Intravenous iron dextran starting at 40 mg/kg BW resulted significant changes in the level of total iron binding capacity compared to control group. In conclusion, intravenous iron dextran significantly altered hepatocyte morphology, increased liver iron concentration, and modified the serum iron profile, reflecting changes that might be observed in patients with transfusion-dependent thalassemia.