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1

An overall view of the process of the regulation of human iron metabolism

100%
Formanowicz D., Formanowicz P.
Biotechnologia
|
2011
|
issue 2
193-207
EN
Iron is a key component of many reactions in the human body, and by virtue of its ability to accept and donate electrons, it is required for a variety of normal cellular functions and is vital for proper growth and development. However, natural iron is rather insoluble and excess of iron is harmful since it can catalyze the formation of oxygen radicals. Fortunately, there are also mechanisms for protecting human body from excess 'free' iron. This is particularly important, given the fact that humans have very limited capacity to excrete iron. Therefore, cells have developed mechanisms to improve the solubility of iron to control intracellular iron concentrations at the point of iron absorption in the small intestine and other tissues. Since the described process is highly complex, a profound understanding of all the relationships occurring among its components is possible when a systems approach is applied to its analysis.
2

Do changes in iron metabolism contribute to the acceleration of the atherosclerosis process?

100%
Formanowicz D.
Biotechnologia
|
2011
|
issue 2
180-192
EN
There are several risk factors whose association with atherosclerosis, a chronic disease with complicated etiology, is well established, including age, gender, smoking, lipids metabolism disorders, diabetes mellitus, obesity and reduced physical activity. Surprisingly, many cardiovascular related deaths occur in individuals without standard risk factors, so it has been suggested that these cases must be the result of other factors, previously not taken into account. This phenomenon resulted in the development of research focused on finding new risk factors. In 1981, Sullivan first postulated the so-called 'iron hypothesis', suggesting that the regular menstrual iron loss, rather than other known effects of estrogen, protects women against coronary heart disease. It is widely believed at present, that iron is an essential catalyst in the oxidation and oxidative modification of low-density lipoprotein cholesterol which appears to be one of the pivotal steps in the early phase of the formation of the atherosclerotic plaque. Thus, iron depletion through menstrual loss might reduce oxidative stress and beneficially affect atherogenesis. Stored iron appears to be essential in the process of atherogenesis which is strictly required for normal cellular metabolism but also serves as a reservoir from which toxic-active iron can be liberated under atherogenic stimuli and result in lipid peroxidation. In this process, two pathways i.e., iron homeostasis metabolic pathway and metabolic pathways involving proinflammatory cytokines are closely interconnected. In human monocytes, these cytokines also increase the uptake of non-transferrin-bound iron, via the stimulation of divalent metal transporter- 1 synthesis and cause iron retention by down-regulating ferroportin synthesis. It has been found recently that iron depositions are prominent in human atherosclerosis lesions. It can therefore be concluded that the results of scientific research, particularly those of the last ten years, provide a strong pathological basis to support the role of iron metabolism alterations in vascular damage and in the progression of atherosclerosis process.
3
Content available remote

Controversies about iron in parkinsonian and control substantia nigra

100%
Galazka-Friedman J., Friedman A.
Acta Neurobiologiae Experimentalis
|
1997
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vol. 57
|
issue 3
217-225
EN
According to the oxidative stress theory iron may play an important role in the pathogenesis of neurodegenerative diseases, as e.g. Parkinson's disease (PD). This review presents the results of studies, obtained by various methods, of iron in substantia nigra (SN) - a cerebral structure which degenerates in PD - and shows controversies concerning the amount of iron, its redox state, and the iron binding compounds. Taking into account all published experimental results, the increase in the concentration of iron in parkinsonian SN vs. control may be estimated as (3 + - 5)%. The presence of large amounts of divalent iron in post mortem SN can be unequivocally negated. It is, however, still possible that iron is involved in the pathogenesis of PD, as even minor changes in the amount and form of iron may initiate processes leading to cells death.
4

Aplication of phytoferritin into food fortification in iron

100%
Zielinska-Dawidziak M.
Biotechnologia
|
2009
|
issue 4
35-39
EN
Various actions have been taken in object to improve human diet in iron with high bioavailibility. One of the new possibility of food fortification is introduction phytoferritin into. In order to do this various strategies are used as increasing of native ferritin supply in human diets as far as application genetic engineering for receiving cultivated plants with high expression of this plant. The most important feature of ferritin introducing into food is its high bioavailability.
5

Pathogenesis and clinical consequences of iron overload in chronic hepatitis C- impact of host and viral factors related to iron metabolism

100%
Sikorska K., Romanowski T., Bielawski K. P.
Biotechnologia
|
2011
|
issue 1
54-65
EN
Chronic hepatitis C virus infection is a leading cause of progressive liver fibrosis, liver cirrhosis and hepatocellular carcinoma. Iron overload is frequently observed in cases of chronic hepatitis C and has been suggested as a negative prognostic factor for this disease. Although the mechanisms leading to iron accumulation are not fully explained yet, both host and viral factors seem to contribute towards the development of this pathology. Better understanding of the interplay between hepatitis C virus replication and expression of iron regulatory molecules may elucidate new and interesting targets for the effective treatment of chronic hepatitis C.
6

Iron - element of life and death

100%
Strozycki P. M.
Biotechnologia
|
1999
|
issue 3
45-61
EN
Iron is the fourth most abundant element and second, after aluminium, metal in the Earth's crust. It is an essential nutrient for almost all living organisms. Iron is a component of hundreds proteins, enzymes and their cofactors. It is a central part of numerous systems, such as: oxygen transport and storage (hemoglobin), elektron transfer (cytochromes), DNA synthesis (ribonucleotide reduction), symbiotic nitrogen fixation (leghemoglobin, nitrogenase), hormone synthesis (i.e. lipoxygenases)... Due to its chemical properties, iron also poses a threat to living cells. It may catalyse one-electron transfer reactions, which (in the presence of active oxygen) generate radical species. Free radicals are the most potent oxidising agents known thus far. The best known effects of their actions include: oxidative DNA damage and lipid peroxidation. These reactions destroy the cell integrity and may lead to its death. Many of the 20th century diseases, like some cancers or heart problems, are in part caused by free radicals. In order to supply with iron and to protect from iron their components, living organisms have developed specific systems for iron acquisition and maintenance in the cell. Despite the potential risks of iron overload, 15% of the world's population suffers iron-deficiency anemia.
7

Role of iron in pathogenesis of Parkinson disease

100%
Galazka-Friedman J., Friedman A.
Biotechnologia
|
2011
|
issue 2
153-158
EN
Parkinson's disease is one of the most frequent human neurodegenerations. Motor symptoms of Parkinson's disease are the consequence of the destruction of nervous cells in the substantia nigra (SN), a small (about 500 mg) structure located deep in human brain. The concentration of iron in SN is comparable to that in liver and is equal to about 180 ? 60 ng/mg of wet tissue and the iron in SN is mostly bound to ferritin. For many years it has been believed that the degeneration of nervous cells in SN in Parkinson's disease is related to an important increase in the concentration of iron. Our own studies based on M?ssbauer spectroscopy and other studies conducted with the use of various techniques have not confirmed this finding. The ratio of the concentration of iron in PD vs. control SN evaluated by Mossbauer spectroscopy was found to be equal 1.00?0.13. We also confirmed that most of iron in SN is located within ferritin. ELISA studies demonstrated a significant decrease in L ferritin in parkinsonian SN compared to the control group. As L-ferritin is related to safe keeping of iron within the ferritin shell, its decrease may lead to an efflux of iron and increase in the concentration of labile iron. Indeed our studies did show a difference in the concentration of labile iron between PD and control SN (135 +- 10 ng/g vs. 76 +- 5 ng/g). This labile iron, which may initiate Fenton reaction, may be the cause of the oxidative stress leading to the death of nervous cells in PD.
8

The role of iron regulatory proteins in the control of iron metabolism in mammals

100%
Stys A., Starzynski R. R., Lipinski P.
Biotechnologia
|
2011
|
issue 1
66-75
EN
The iron regulatory proteins (IRP1 and IRP2) are two cytoplasmic RNA-binding proteins involved in the mechanisms that control iron metabolism in mammalian cells. They modulate the expression of iron-related proteins at a post-transcriptional level by binding to specific iron regulatory elements (IREs) on their mRNAs. IRP-IRE interaction can block protein synthesis or stabilize the mRNA. At low intracellular iron concentration, IRPs bind to the IRE of ferritin or ferroportin mRNAs and block their translation. Direct interactions between IRPs and several IRE motifs stabilize transferrin receptor mRNA. The converse regulation of ferritin and TfR synthesis, being a consequence of the lack of binding of IRPs to IRE, occurs in cells with high iron level. Thus, IRP-mediated regulation rapidly restores the physiological level of iron during its deficiency as well as excess. The role of IRPs in maintaining the intracelluar iron balance has been relatively well characterized in numerous types of mammalian cells. However, the importance of IRPs in the regulation of systemic iron metabolism in mammals, particularly, in signaling between the cells which play major roles in body iron metabolism, such as duodenal enterocytes, reticuloendothelial macrophages, hepatocytes, and bone marrow precursors of red blood cells, is only beginning to be investigated. Several studies have shown that IRP2 is a predominant regulator of iron homeostasis in mice housed under standard conditions, thus limiting the impact of IRP1 on this metabolic pathway. Although IRP1-deficient mice do not display a strong pathological phenotype, a deletion of both IRPs is embryonic lethal. In addition, in vitro and in vivo studies have reported that nitric oxide (NO) and hydrogen peroxide (H2O2), which are produced during inflammation, are potent IRP1 regulators that mediate the disassembly of Fe-S cluster of IRP1. There is also an increasing evidence that NO and superoxide anion (O2 @!) may induce a strong down-regulation of IRP1 at the protein level and thus have an impact on the binding of IRP1 to IREs. All these data suggest a predominant role of IRP1 in the regulation of iron homeostasis under specific physiopathological conditions.
9

Effect of converting enzyme inhibitor on copper and iron concentrations of blood plasma in calves during the neonatal period

88%
Skrzypczak W., Dratwa-Chalupnik A., Ozgo M., Michalerk K., Lepczynski A., Hejza K., Siwa J.
Folia Biologica
|
2010
|
vol. 58
|
issue 1-2
119-124
EN
The converting enzyme catalyzes the conversion of angiotensin I to angiotensin II. Ang II is the key component of the renin-angiotensin-aldosterone (RAA) system, regulating water-electrolyte balance in newborn calves. Captopril is an inhibitor of the angiotensin-converting enzyme. The aim of this study was to examine the effect of captopril-induced reduction of convertase activity on copper and iron concentrations of blood plasma in calves. The experiment was carried out on 10 Holstein-Friesian female calves, during the first week of life. Copper and iron concentrations in blood plasma were examined before and after captopril administration (0.5, 1, 2, 4, and 6 hours after giving the inhibitor) on subsequent days of the experimental period. The results demonstrated that the copper concentration of blood plasma increased with age. On the seventh day, the copper concentration stabilised at the level observed in adult cattle. Measured before captopril administration, the iron concentration in blood plasma changed: the highest iron concentration was observed on the first day of life, which was followed by a decrease on the third day, and thereafter an increase on the seventh day. These changes may significantly influence the neonatal adaptation of newborn calves, particularly hemopoiesis efficiency. Captopril did not cause statistically significant changes in plasma copper concentration in calves. However, the reduction of angiotensin convertase activity induced by captopril administration resulted in a drop of plasma iron concentration, observed already within 1-2 hours after administration of the inhibitor, and especially within two days post partum. The results indicate that an efficient mechanism maintaining a constant concentration of selected minerals may involve changes in the reabsorption of these minerals from the system fluids to tissues.
10

Distribution of the Fe (II) and Fe (III) dissolved in the interstitial water of the Gulf of Gdansk

88%
Bialkowska I., Bolalek B. J., Bolalek J.
Oceanological Studies
|
2000
|
vol. 29
|
issue 4
43-54
EN
A sediment environment of the Gulf of Gdansk is reductive to the iron (III). The iron (II) is a dominant form of this element in the interstitial water, and a total reduction takes place in a sediment layer of up to 20 cm. A speciation of a dissolved iron as well as a total iron concentration is related to types of sediments in a measuring point. It could also be noted that a concentration of each iron form in the above-bottom water layer is much lower than in the interstitial water of the top sediment layer. To illustrate redox conditions in the environment a ratio Fe(III) : Fe(II) was introduced. In the waters, the iron (III) dominates and the Fe(III) : Fe(II) ratio is much higher than the relevant value in the interstitial water.
11

Interdependence between phosphorus forms in sediments and iron in interstitial waters in the Gulf of Gdansk

88%
Matuszewska K., Bialkowska I., Bolalek J.
Oceanological and Hydrobiological Studies
|
2003
|
issue 1
5-14
EN
The content of various phosphorus forms in sediments and the content of iron in interstitial waters were measured in sediment samples collected in the Gulf of Gdansk in March 2001. The studies showed that the greatest amounts of the total phosphorus and total dissolved iron were present in the uppermost sediment layer, and their respective concentrations ranged from 203,99 mumol?g-1d.w. to 1894,02 mumol?g-1d.w., and from 0,02 mumol?dm-3 to 4,68 mumol?dm-3. The contents of these parameters were directly connected with the type of sediment - the greatest concentrations were measured in fine sediments. The analysis of multiple correlation coefficients demonstrated that in over 90% of cases the concentration of phosphorus bound with iron depended on: the sediment type and its humidity, the content of organic matter, and the concentration of the total iron dissolved in the interstitial waters.
12

Therapeutic potential of heme oxygenase-1 in cardiovascular disease

88%
Jazwa A., Florczyk U., Stepniewski J., Jozkowicz A., Dulak J.
Biotechnologia
|
2011
|
issue 2
166-179
EN
Heme oxygenase-1 (HO1) degrades heme to carbon monoxide (CO), biliverdin, and ferrous iron. Through these products, HO1 mitigates cellular injury by exerting anti-oxidant, anti-apoptotic, and anti-inflammatory effects. Several lines of evidence indicate that angiogenic factors, such as vascular endothelial growth factor A (VEGF) and stromal cell-derived factor 1 (SDF1), mediate their proangiogenic action in endothelial cells and endothelial progenitor cells through induction of HO1, and reciprocally, VEGF and SDF1 are enhanced by HO1 overexpression. Ferrous iron released during the breakdown of free heme by HO1 is an extremely pro-oxidative molecule that can be rapidly removed by ferritin. Of note, this iron sequestering protein also has been shown to exert some proangiogenic effects. Moreover, our recent data indicate that HO1 is an important mediator of differentiation and function of stem cells, including endothelial and myoblasts progenitors. All of this makes HO1 a promising target for novel cardiovascular therapies. The aim of this review is to discuss the existing knowledge and to propose the therapeutic approaches, which have to consider the necessity of tight regulation of HO1 expression.
13

Procedure for radiochemical analysis of 55Fe and 63Ni in selected environmental samples

88%
Skwarzec B.
Oceanological Studies
|
1996
|
vol. 25
|
issue 3
15-23
EN
Radiochemical procedures are described for the determination of iron 55Fe and nickel 63Ni isotopes in environmental samples. The methods were based on the mineralisation of sediment and biological material, coprecipitation and separation of iron and nickel on anion exchange resin. The separated isotopes were electroplated onto a copper disc and their activi-ties was measured by beta spectrometry using an anti-coincidence GM gas flow counter. The proposed procedures were tested on samples from the Baltic Sea. The concentration of 55Fe in reactor water samples falls within the range from 0.15 to 2185 Bq ?1-1,while in brown algae Fucus vesiculosus it lies between 0.13 and 3.50 Bq ? kg-1 dry wt. The 63Ni is non-uniformly distributed within the Baltic fish. More than 95% of the total 63Ni content in cod and herring is located in fillet with skin and scale.
14
Content available remote

Inhibition of neuronal nitric oxide synthase prevents iron-induced cerebellar Purkinje cell loss in the rat

88%
Gulturk S., Kozan R., Bostanci M. O., Sefil F., Bagirici F.
Acta Neurobiologiae Experimentalis
|
2008
|
vol. 68
|
issue 1
26-31
EN
Iron plays an important role in maintaining normal brain function. However, in many neurodegenerative diseases abnormal iron accumulation in specific brain regions has been consistently reported. In this study, we investigated the neurotoxic effect of the intracerebroventricularly injected iron on the cerebellar Purkinje cells in the rat and the role of nitric oxide (NO) in this process. The role of NO in rats administered iron (FeCl36H2O) was examined with the use of a donor of NO, L-arginine (L-Arg), and a central selective inhibitor of NO synthase, 7-nitroindazole (7-NI). For this reason, rats were divided into 5 groups: control, iron-injected, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI. Means (value ? standard deviation) of the total numbers of Purkinje cells in the cerebellum were estimated as 337 ? 23, 209 ? 16, 167 ? 19, 305 ? 26, and 265 ? 14 thousands in the control, iron, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI groups, respectively. Iron treatment alone and the combination of iron and L-Arg caused a significant reduction in the total number of cerebellar Purkinje cells. Therefore, L-Arg increased the Purkinje cell loss induced by treatment with iron. These data show that inhibition of the neuronal NOS by 7-NI can prevent some of the deleterious effects of iron on cerebellar Purkinje cells. Presence of L-arginine decreased the neuroprotective effect of 7-NI.
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