Iron Dextran

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.

Iron overload drives oxidative stress and vascular injury, yet the role of hydrogen sulfide (H 2 S) in systemic and vascular iron regulation remains unclear. We investigated how cystathionine γ‐lyase (CSE)‐derived H 2 S influences iron handling and vascular responses following acute iron overload. Wild‐type (WT) and CSE‐knockout (CSE‐KO) mice received PBS, low‐concentration (1×) or high‐concentration (3×) iron dextran intravenously. CSE‐KO mice exhibited elevated serum iron and transferrin saturation but impaired ferritin upregulation compared to WT. KO aortas showed greater iron deposition, elastin degradation, and inflammatory remodeling under high iron. Iron overload impaired phenylephrine‐induced vasocontraction and H 2 S‐mediated vasorelaxation, with CSE‐KO mice displaying the most severe vascular dysfunction and elevated blood pressure. WT mice compensated via CSE upregulation and increased H 2 S production. Our findings demonstrate that CSE/H 2 S deficiency disrupts ferritin‐mediated iron storage, exacerbates vascular iron accumulation, and worsens vasomotor dysfunction during iron overload. The CSE/H 2 S pathway may represent a therapeutic target for mitigating iron‐induced vascular damage.