Experimental animal model to study iron overload and iron chelation and review of other such models

Iron overload in patients with myelodysplastic syndromes: An updated overview

“…13,14 It is also known that iron deficiency and hypoxia stimulate the transcription of DMT1 and ferroportin messenger RNA through hypoxiainducible factors that are released by the action of iron regulatory proteins and iron-responsive elements, leading to increased iron efflux at the level of macrophages and enterocytes. 17 Hereditary hemochromatosis results from genetic abnormalities affecting one of those regulatory molecules, most commonly HFE and transferrin receptor genes, 18 whereas transfusional iron overload, in addition to hepatic and renal diseases, is among the most common causes of acquired iron overload. 16 Thus, ferroportin, the only iron exporter, is regulated at the translational level by iron and at the transcriptional level by heme.…”

“…15 Iron regulatory proteins bind to iron-responsive elements in low-iron conditions, and dissociate from those with iron excess. 18 Nonetheless, acquired non-transfusional iron overload can be related to abnormalities involving GDF15 and TWSG1. 17 Hereditary hemochromatosis results from genetic abnormalities affecting one of those regulatory molecules, most commonly HFE and transferrin receptor genes, 18 whereas transfusional iron overload, in addition to hepatic and renal diseases, is among the most common causes of acquired iron overload.…”

“…17 Hereditary hemochromatosis results from genetic abnormalities affecting one of those regulatory molecules, most commonly HFE and transferrin receptor genes, 18 whereas transfusional iron overload, in addition to hepatic and renal diseases, is among the most common causes of acquired iron overload. 18 The pathological effect of iron overload is mediated by non-transferrin-bound iron and its loosely protein-bound fraction labile plasma iron (LPI), which at high levels might be toxic to various tissues through the production of reactive oxygen species (ROS). 7 The excess iron, whether inherited or acquired, is deposited in different vital organs, especially when the total body iron exceeds 7 g, leading to multiple clinical consequences including cardiomyopathy, cirrhosis, diabetes mellitus, hypogonadism, and joint disease.…”

Cyclic Hydroxamic Acid Analogues of Bacterial Siderophores as Iron‐Complexing Agents prepared through the Castagnoli–Cushman Reaction of Unprotected Oximes

“…[11] Such an approachh olds ag reat promise for circumventing drug resistantb acterial defense mechanism as well as for in vivo imaging and eradication of bacterial colonies (teranostics). [13] Collectively, the vast applications of cyclic hydroxamic acids in biomedical science justifyt he development of new,f lexible synthetic approachestot his importantclass of heterocyclic compounds. [13] Collectively, the vast applications of cyclic hydroxamic acids in biomedical science justifyt he development of new,f lexible synthetic approachestot his importantclass of heterocyclic compounds.…”

Iron Overload Effect on Serum Levels of Glucose, Insulin and HOMA-IR was Ifluenced by the Type of Fat in Female Sprague-Dawley Rats Fed High-Fat-Diets

“…Rats were kept on their respective diet. Iron was supplemented by intraperitonial injections as two doses of iron sucrose: dose1 (Do1); 15 mg/kg body weight (BW) and dose 2(Do2); (75 mg/kg BW), three times per week, for 4 consecutive weeks [25][26][27]. In control group, rats received an equivalent volume of sterile saline After which, rats were sacrificed by chloroform anesthesia, after 12 hours fasting.…”