Journal of Trace Elements in Medicine and Biology ( IF 3.6 ) Pub Date : 2020-05-15 , DOI: 10.1016/j.jtemb.2020.126550 Agnieszka Ścibior 1 , Iwona Hus 2 , Joanna Mańko 3 , Dariusz Jawniak 3
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Background
The current knowledge about the effects of vanadium (V) on iron (Fe)-related proteins and Fe homeostasis (which is regulated at the systemic, organelle, and cellular levels) is still insufficient.
Objective
This fact and our earlier results prompted us to conduct studies with the aim to explain the mechanism of anemia accompanied by a rise in hepatic and splenic Fe deposition in rats receiving sodium metavanadate (SMV) separately and in combination with magnesium sulfate (MS).
Results
We demonstrated for the first time that SMV (0.125 mg V/mL) administered to rats individually and in conjunction with MS (0.06 mg Mg/mL) for 12 weeks did not cause significant differences in the hepatic hepcidin (Hepc) and hemojuvelin (HJV) concentrations, compared to the control. In comparison with the control, there were no significant changes in the concentration of transferrin receptor 1 (TfR1) in the liver of rats treated with SMV and MS alone (in both cases only a downward trend of 14% and 15% was observed). However, a significant reduction in the hepatic TfR1 level was found in rats receiving SMV and MS simultaneously. In turn, the concentration of transferrin receptor 2 (TfR2) showed an increasing trend in the liver of rats treated with SMV and/or MS.
Conclusions
The experimental data suggest that the pathomechanism of the SMV-induced anemia is not associated with the effect of V on the concentration of Hepc in the liver, as confirmed by the unaltered hepatic HJV and TfR1 levels. Therefore, further studies are needed in order to check whether anemia that developed in the rats at the SMV administration (a) results from the inhibitory effect of V on erythropoietin (EPO) production, (b) is related to the effect of V on the induction of matriptase-2 (TMPRSS6) expression, or (c) is associated with the influence of this metal on haem synthesis.
中文翻译：
评估单独/联合施用钒和镁期间大鼠肝脏中选定的铁相关蛋白/受体的水平。
背景
目前关于钒 (V) 对铁 (Fe) 相关蛋白和铁稳态（在全身、细胞器和细胞水平上进行调节）的影响的知识仍然不足。
客观的
这一事实和我们早期的结果促使我们进行研究，旨在解释单独接受偏钒酸钠 (SMV) 和联合硫酸镁 (MS) 的大鼠贫血伴随肝和脾铁沉积增加的机制。
结果
我们首次证明，单独给予大鼠 SMV（0.125 mg V/mL）以及与 MS（0.06 mg Mg/mL）联合给药 12 周不会导致肝铁调素 (Hepc) 和血幼素 (HJV) 的显着差异。 ）浓度，与对照相比。与对照组相比，单独使用SMV和MS治疗的大鼠肝脏中转铁蛋白受体1（TfR1）的浓度没有显着变化（在两种情况下仅观察到14％和15％的下降趋势）。然而，同时接受 SMV 和 MS 的大鼠肝脏 TfR1 水平显着降低。反过来，接受 SMV 和/或 MS 治疗的大鼠肝脏中转铁蛋白受体 2 (TfR2) 的浓度显示出增加的趋势。
结论
实验数据表明，SMV 引起的贫血的病理机制与 V 对肝脏中 Hepc 浓度的影响无关，这一点已由未改变的肝脏 HJV 和 TfR1 水平证实。因此，需要进一步的研究来检查 SMV 给药时大鼠中出现的贫血是否是由 V 对促红细胞生成素 (EPO) 产生的抑制作用引起的，(b) 是否与 V 对促红细胞生成素 (EPO) 产生的影响有关。诱导 matriptase-2 (TMPRSS6) 表达，或 (c) 与该金属对血红素合成的影响有关。
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