Evaluation of the level of selected iron-related proteins/receptors in the liver of rats during separate/combined vanadium and magnesium administration

Ścibior, Agnieszka; Hus, Iwona; Mańko, Joanna; Jawniak, Dariusz

doi:10.1016/j.jtemb.2020.126550

Cited by 5 publications

(5 citation statements)

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“…This hormone inhibits ferroportindependent iron efflux from enterocytes, hepatocytes, and macrophages into the plasma [21]. An increase of 16% in hepatic ferroportin has been found in rats treated with sodium metavanadate [23], consistent with the results obtained at the present conditions in hepatic cells (Figure 2). The results obtained in the present study showed that the decrease in hepcidin level facilitated an increase in the expression of the ferroportin transporter, thereby allowing a larger efflux of Fe into the plasma (Table 3).…”

Section: Effect Of V(iv) Treatment On the Mrna Expression Level Of Hepcidin In Liver And Level Of Fe Transferrin And Ferritin In Serum Ansupporting

confidence: 90%

“…Accordingly, the present study aimed to examine whether the treatment of diabetic rats with V causes hematological changes and whether such changes are related to changes in hepcidin expression and the secretion of pro-inflammatory factors, previously demonstrated in healthy rats [22,23]. This study may help clarify the role of V as a micronutrient and its biological activity, potential pharmacological applications, and toxicity.…”

Section: Introductionmentioning

confidence: 91%

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Vanadium Decreases Hepcidin mRNA Gene Expression in STZ-Induced Diabetic Rats, Improving the Anemic State

et al. 2021

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Diabetes is a disease with an inflammatory component that courses with an anemic state. Vanadium (V) is an antidiabetic agent that acts by stimulating insulin signaling. Hepcidin blocks the intestinal absorption of iron and the release of iron from its deposits. We aim to investigate the effect of V on hepcidin mRNA expression and its consequences on the hematological parameters in streptozotocin-induced diabetic Wistar rats. Control healthy rats, diabetic rats, and diabetic rats treated with 1 mgV/day were examined for five weeks. The mineral levels were measured in diet and serum samples. Hepcidin expression was quantified in liver samples. Inflammatory and hematological parameters were determined in serum or whole blood samples. The inflammatory status was higher in diabetic than in control rats, whereas the hematological parameters were lower in the diabetic rats than in the control rats. Hepcidin mRNA expression was significantly lower in the V-treated diabetic rats than in control and untreated diabetic rats. The inflammatory status remained at a similar level as the untreated diabetic group. However, the hematological profile improved after the V-treatment, reaching similar levels to those found in the control group. Serum iron level was higher in V-treated than in untreated diabetic rats. We conclude that V reduces gene expression of hepcidin in diabetic rats, improving the anemic state caused by diabetes.

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Section: Effect Of V(iv) Treatment On the Mrna Expression Level Of Hepcidin In Liver And Level Of Fe Transferrin And Ferritin In Serum Ansupporting

confidence: 90%

Section: Introductionmentioning

confidence: 91%

Vanadium Decreases Hepcidin mRNA Gene Expression in STZ-Induced Diabetic Rats, Improving the Anemic State

et al. 2021

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“…Transferrin is a blood-plasma glycoprotein that plays a central role in iron metabolism and is responsible for ferric-ion delivery [130]. In an animal study, the concentration of the transferrin receptor 2 (TfR2) showed an increasing trend in the liver of rats treated with Mg sulfate [131]. In addition, the Ca signaling through the CAMKK2 and CAMK4 (calcium/calmodulin-dependent protein kinase kinase) proteins affects transferrin proteinmediated iron transport [132].…”

Section: Magnesium and Its Associationsmentioning

confidence: 99%

Magnesium Status and Calcium/Magnesium Ratios in a Series of Cystic Fibrosis Patients

et al. 2022

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Magnesium (Mg) is an essential micronutrient that participates in various enzymatic reactions that regulate vital biological functions. The main aim was to assess the Mg status and its association with nutritional indicators in seventeen cystic fibrosis (CF) patients. The serum Mg and calcium (Ca) levels were determined using standardized methods and the dietary Mg intake by prospective 72 h dietary surveys. The mean serum Ca (2.45 mmol/L) and Mg (0.82 mmol/L) had normal levels, and the mean dietary intake of the Ca (127% DRI: Dietary Reference Intake) and Mg (125% DRI) were high. No patients had an abnormal serum Ca. A total of 47% of the subjects had hypomagnesemia and 12% insufficient Mg consumption. One patient had a serum Mg deficiency and inadequate Mg intake. A total of 47 and 82% of our series had a high serum Ca/Mg ratio of >4.70 (mean 4.89) and a low Ca/Mg intake ratio of <1.70 (mean 1.10), respectively. The likelihood of a high Ca/Mg ratio was 49 times higher in patients with a serum Mg deficiency than in normal serum Mg patients. Both Ca/Mg ratios were associated with the risk of developing cardiovascular disease (CVD), type 2 diabetes (T2D), metabolic syndrome (MetS), and even several cancers. Therefore, 53% of the CF patients were at high risk of a Mg deficiency and developing other chronic diseases.

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“…Livers were obtained from some outbred albino male Wistar rats used in our previous experiments, in which all the animals were divided into 4 groups and maintained individually in stainless steel cages in a room with controlled conditions. During the whole experiment, all rats received ( ad libitum ) properly balanced standard granulated laboratory rodent chow (Labofeed B, Fodder and Concentrate Factory, Kcynia, Poland) and appropriate fluids to drink every day over a 12-week period in special bottles with a scale [ 31 ]: control—deionized water (12-15 rats/per group), SMV—sodium metavanadate (12-15 rats/per group) at a concentration of 0.125 mg V/mL (pH = 7.2), MS—magnesium sulfate (10-12 rats/per group) at a concentration of 0.06 mg Mg/mL (pH = 5.7), and SMV+MS—14-15 rats/per group at a concentration of 0.125 mg V + 0.06 mg Mg/mL (pH = 7.1). As described previously [ 32 ], the intake of food, deionized water, and the SMV, MS, and SMV+MS water solutions was monitored daily throughout the experimental period, and body weight was checked weekly.…”

Section: Methodsmentioning

confidence: 99%

“…Then, the wet weights were recorded, and the samples were stored at -80°C until the planned analyses. The experiment was conducted in accordance with the experimental protocol approved by the 1 st Local Ethical Committee for Animal Studies in Lublin [ 31 ].…”

Section: Methodsmentioning

confidence: 99%

Response of Cytoprotective and Detoxifying Proteins to Vanadate and/or Magnesium in the Rat Liver: The Nrf2‐Keap1 System

Ścibior

Wojda

Wnuk

et al. 2021

Oxidative Medicine and Cellular Longevity

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Oxidative stress (OS) is a mechanism underlying metal-induced toxicity. As a redox-active element, vanadium (V) can act as a strong prooxidant and generate OS at certain levels. It can also attenuate the antioxidant barrier and intensify lipid peroxidation (LPO). The prooxidant potential of V reflected in enhanced LPO, demonstrated by us previously in the rat liver, prompted us to analyze the response of the nuclear factor erythroid-derived 2-related factor 2/Kelch-like ECH-associated protein 1 (Nrf2-Keap1) system involved in cellular regulation of OS to administration of sodium metavanadate (SMV, 0.125 mg V/mL) and/or magnesium sulfate (MS, 0.06 mg Mg/mL). The levels of some Nrf2-dependent cytoprotective and detoxifying proteins, i.e., glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), glutamate cysteine ligase catalytic subunit (GCLC), glutathione synthetase (GSS), NAD(P) H dehydrogenase quinone 1 (NQO1), UDP-glucumno-syltransferase 1 (UGT1), and heme oxygenase 1 (HO-1); glutathione (GSH); metallothionein (MT1); and glutamate-cysteine ligase (GCL) mRNA were measured. We also focused on the V-Mg interactive effects and trends toward interactive action as well as relationships between the examined indices. The elevated levels of Nrf2, GCL mRNA, and GCL catalytic subunit (GCLC) confirm OS in response to SMV and point to the capacity to synthesize GSH. The results also suggest a limitation of the second step in GSH synthesis reflected by the unchanged glutathione synthetase (GSS) and GSH levels. The positive correlations between certain cytoprotective/detoxifying proteins (which showed increasing trends during the SMV and/or MS administration, compared to the control) and between them and malondialdehyde (MDA), the hepatic V concentration/total content, and/or V dose (discussed by us previously) point to cooperation between the components of antioxidant defense in the conditions of the hepatic V accumulation and SMV-induced LPO intensification. The V-Mg interactive effect and trend are involved in changes in Nrf2 and UGT1, respectively. The p62 protein has to be determined in the context of potential inhibition of degradation of Keap1, which showed a visible upward trend, in comparison with the control. The impact of Mg on MT1 deserves further exploration.

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Evaluation of the level of selected iron-related proteins/receptors in the liver of rats during separate/combined vanadium and magnesium administration

Cited by 5 publications

References 129 publications

Vanadium Decreases Hepcidin mRNA Gene Expression in STZ-Induced Diabetic Rats, Improving the Anemic State

Vanadium Decreases Hepcidin mRNA Gene Expression in STZ-Induced Diabetic Rats, Improving the Anemic State

Magnesium Status and Calcium/Magnesium Ratios in a Series of Cystic Fibrosis Patients

Response of Cytoprotective and Detoxifying Proteins to Vanadate and/or Magnesium in the Rat Liver: The Nrf2‐Keap1 System

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