
MedChemExpress - Model Ferric nitrilotriacetate - 16448-54-7
Ferric nitrilotriacetate (Fe-NTA), a complexation of nitriloacetic acid with iron, is a highly reactive compound used to induce degenerative disorders through oxidative stress (OS). Ferric nitrilotriacetate is also used in several studies to induce hyperglycemia, glycosuria, and both renal and liver carcinogenesis[1].MCE products for research use only. We do not sell to patients.
Ferric nitrilotriacetate
MCE China:Ferric nitrilotriacetate
Brand:MedChemExpress (MCE)
Cat. No.HY-145157
CAS:16448-54-7
Purity:98.0%
Storage:4°C, stored under nitrogen *In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Shipping:Room temperature in continental US; may vary elsewhere.
Description:Ferric nitrilotriacetate (Fe-NTA), a complexation of nitriloacetic acid with iron, is a highly reactive compound used to induce degenerative disorders through oxidative stress (OS). Ferric nitrilotriacetate is also used in several studies to induce hyperglycemia, glycosuria, and both renal and liver carcinogenesis.
In Vivo:Ferric nitrilotriacetate can be used in animal modeling to create renal tumor and diabetes models. After intraperitoneal injection into mice, it deposits heavily in the liver and pancreas[1][2][3][4]. .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction of renal tumors[3] Background Ferric nitrilotriacetate can induce oxidative stress, leading to lipid peroxidation of renal cell membranes and DNA damage, thereby promoting the development of renal tumors[1][2]. Specific Mmodeling Methods Mice: A/J • male • 4-week-oldAdministration: 1.8-2.7 mg of Fe/kg • ip • once daily, 6 days a week for 12 weeks Note 1.8 to 2.7 mg refers to the amount of Fe contained in ferric nitrilotriacetate. Modeling Indicators Pathological Changes: The renal proximal tubular (PCT) cells in mice exhibit degeneration, necrosis, and shedding. Many PCT cells show regenerative characteristics, with some regenerative cells being abnormally large and featuring prominent nucleoli and mitoses. Some regenerative cells lack tubular formation.Phenotypic Observations: Renal tubular cell tumors develop. The appearance of renal tumors includes solid, cystic, or hemorrhagic forms. Microscopic examination reveals tumor cells with clear, granular, or spindle shapes, forming solid aggregates, papillae, cysts, or glandular patterns. Correlated Product(s): / Opposite Product(s): / .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction of diabetes[4] Background Ferric nitrilotriacetate causes significant iron deposition in the pancreas, leading to oxidative stress through the generation of reactive oxygen species (ROS) and free radicals. This results in damage and functional failure of pancreatic islet β-cells, reducing insulin secretion and consequently inducing diabetes.[4]. Specific Mmodeling Methods Rat: Wistar • male and femaleAdministration: 200 mg/rat • ip • once daily, Specifics of the administration method are detailed in the note Note Rats received intraperitoneal injections of Ferric nitrilotriacetate, with each rat receiving a total of approximately 200 mg of iron. The dosage and frequency of administration were as follows:Weeks 1-3: 2 mg Fe/kg, once daily; Weeks 3-6: 6 mg Fe/kg, once daily; Next 2 months: 10 mg Fe/kg, once daily. Modeling Indicators Pathological Changes: Significant iron deposition was observed in the exocrine cells of the pancreas in mice, with a reduction in insulin-storing β granules in the islet β cells and a decrease in zinc ion content.Phenotypic Observations: Mice exhibited diabetic symptoms, including hyperglycemia, glycosuria, ketonemia, and ketonuria. 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References:
[1]. Joël Essogo J, et al. Zanthoxylum heitzii Modulates Ferric Nitrilotriacetate-Dependent Oxidative Alterations in Four Vital Organs: An In Vitro Organoprotective Model. Evid Based Complement Alternat Med. 2017;2017:6058150. [Content Brief]
[2]. Inoue S, et al. Hydroxyl radical production and human DNA damage induced by ferric nitrilotriacetate and hydrogen peroxide. Cancer Res. 1987 Dec 15;47(24 Pt 1):6522-7. [Content Brief]
[3]. Li JL, et al. Subacute nephrotoxicity and induction of renal cell carcinoma in mice treated with ferric nitrilotriacetate. Cancer Res. 1987 Apr 1;47(7):1867-9. [Content Brief]
[4]. Awai M, et al. Induction of diabetes in animals by parenteral administration of ferric nitrilotriacetate. A model of experimental hemochromatosis. Am J Pathol. 1979 Jun;95(3):663-73. PMID: 377994; [Content Brief]
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