scholarly journals The Role of GSH in Intracellular Iron Trafficking

2021 ◽  
Vol 22 (3) ◽  
pp. 1278
Author(s):  
Robert Hider ◽  
Mayra Vera Aviles ◽  
Yu-Lin Chen ◽  
Gladys Oluyemisi Latunde-Dada
Keyword(s):  
Ternary Complexes ◽  
Physiological Significance ◽  
Intracellular Iron ◽  
Kidney Physiology ◽  
Iron Trafficking ◽  
Binding Capability ◽  
Iron Pool

Evidence is reviewed for the role of glutathione in providing a ligand for the cytosolic iron pool. The possibility of histidine and carnosine forming ternary complexes with iron(II)glutathione is discussed and the physiological significance of these interactions considered. The role of carnosine in muscle, brain, and kidney physiology is far from established and evidence is presented that the iron(II)-binding capability of carnosine relates to this role.

scholarly journals The 58-Kilodalton Major Virulence Factor of Francisella tularensis Is Required for Efficient Utilization of Iron

2009 ◽  
Vol 77 (10) ◽  
pp. 4429-4436 ◽  
Author(s):  
Helena Lindgren ◽  
Marie Honn ◽  
Igor Golovlev ◽  
Konstantin Kadzhaev ◽  
Wayne Conlan ◽  
...  
Keyword(s):  
Francisella Tularensis ◽  
Iron Acquisition ◽  
Protein A ◽  
Intracellular Iron ◽  
Major Virulence Factor ◽  
Iron Pool ◽  
Isogenic Mutants ◽  
Schu S4 ◽  
Iron Concentrations

ABSTRACT We investigated the role of the 58-kDa FTT0918 protein in the iron metabolism of Francisella tularensis. The phenotypes of SCHU S4, a prototypic strain of F. tularensis subsp. tularensis, and the ΔFTT0918 and ΔfslA isogenic mutants were analyzed. The gene product missing in the ΔfslA mutant is responsible for synthesis of a siderophore. When grown in broth with various iron concentrations, the two deletion mutants generally reached lower maximal densities than SCHU S4. The ΔFTT0918 mutant, but not the ΔfslA mutant, upregulated the genes of the F. tularensis siderophore locus (fsl) operon even at high iron concentrations. A chrome azurol sulfonate plate assay confirmed siderophore production by all strains except the ΔfslA strain. In a cross-feeding experiment using medium devoid of free iron, SCHU S4 promoted growth of the ΔfslA strain but not of the ΔFTT0918 strain. The sensitivity of SCHU S4 and the ΔFTT0918 and ΔfslA strains to streptonigrin demonstrated that the ΔFTT0918 strain contained a smaller free intracellular iron pool and that the ΔfslA strain contained a larger one than SCHU S4. In contrast to the marked attenuation of the ΔFTT0918 strain, the ΔfslA strain was as virulent as SCHU S4 in a mouse model. Altogether, the data demonstrate that the FTT0918 protein is required for F. tularensis to utilize iron bound to siderophores and that it likely has a role also in siderophore-independent iron acquisition. We suggest that the FTT0918 protein be designated Fe utilization protein A, FupA.

Intracellular iron trafficking: role of cytosolic ligands

BioMetals ◽  
2012 ◽  
Vol 25 (4) ◽  
pp. 711-723 ◽  
Author(s):  
Maya Shvartsman ◽  
Z. Ioav Cabantchik
Keyword(s):  
Intracellular Iron ◽  
Iron Trafficking

scholarly journals The Role of Iron in the Pathogenesis of Atherosclerosis

2017 ◽  
pp. S55-S67 ◽  
Author(s):  
P. KRAML
Keyword(s):  
Cardiovascular Risk ◽  
Free Oxygen Radicals ◽  
Intracellular Iron ◽  
Iron Storage ◽  
Oxidation Stress ◽  
Iron Stores ◽  
Labile Iron Pool ◽  
Labile Iron ◽  
Iron Pool

Ferritin and increased iron stores first appeared on the list of cardiovascular risk factors more than 30 years ago and their causal role in the pathogenesis of atherosclerosis has been heavily discussed since the early 1990s. It seems that besides traditional factors such as hyperlipoproteinemia, hypertension, diabetes mellitus, obesity, physical inactivity, smoking and family history, high iron stores represent an additional parameter that could modify individual cardiovascular risk. The role of iron in the pathogenesis of atherosclerosis was originally primarily associated with its ability to catalyze the formation of highly reactive free oxygen radicals and the oxidation of atherogenic lipoproteins. Later, it became clear that the mechanism is more complex. Atherosclerosis is a chronic fibroproliferative inflammatory process and iron, through increased oxidation stress as well as directly, can control both native and adaptive immune responses. Within the arterial wall, iron affects all of the cell types that participate in the atherosclerotic process (monocytes/macrophages, endothelial cells, vascular smooth muscle cells and platelets). Most intracellular iron is bound in ferritin, whereas redox-active iron forms labile iron pool. Pro-inflammatory and anti-inflammatory macrophages within arterial plaque differ with regard to the amount of intracellular iron and most probably with regard to their labile iron pool. Yet, the relation between plasma ferritin and intracellular labile iron pool has not been fully clarified. Data from population studies document that the consumption of meat and lack of physical activity contribute to increased iron stores. Patients with hereditary hemochromatosis, despite extreme iron storage, do not show increased manifestation of atherosclerosis probably due to the low expression of hepcidin in macrophages.

IRON METABOLISM AND INDICATORS REFLECTING ITS CHANGES IN PULMONARY TUBERCULOSIS (REVIEW OF LITERATURE)

2020 ◽  
Vol 65 (3) ◽  
pp. 149-154
Author(s):  
E. A. Borodulina ◽  
E. V. Yakovleva
Keyword(s):  
Pulmonary Tuberculosis ◽  
Hiv Infection ◽  
Iron Metabolism ◽  
Essential Element ◽  
The Body ◽  
Cellular Respiration ◽  
Bacterial Cells ◽  
Intracellular Iron ◽  
Iron Pool

Iron is an essential element for human and bacteria, including mycobacterium tuberculosis. Over review includesthe literature on the problem of iron metabolism in patients with tuberculosis and with comorbid pathology HIV infection and tuberculosis. The literature was searched for when writing this review using the RSCI, CyberLeninka, Scopus, Web of Science, MedLine, PubMed databases using the following keywords: iron, ferritin, hepsidin, lactoferrin, tuberculosis, pneumonia, HIV infection. Iron compounds are involved in many redox reactions: oxygen transport, cellular respiration, the trichloroacetic acid cycle, DNA biosynthesis, and others. The ratio of intracellular and extracellular iron in the body is regulated by the low molecular weight hormone hepcidin, the mechanism of action of which is to block the function of ferroportin, an exporter of iron from cells, which leads to the accumulation of the intracellular iron pool and the prevention of the toxic effect of free iron. The role of iron in the interaction of the human body with ferro-dependent bacteria has been established. Iron is necessary for the growth and development of bacterial cells, and the methods for its production from the host are different. Information on the effect of iron metabolism on pulmonary tuberculosis is scarce and contradictory: some authors have identified a decrease in hemoglobin and transferrin in combination with elevated levels of ferritin in patients with tuberculosis; according to other sources, hyperferritinemia in tuberculosis cannot be predictive, but is a marker inflammation. At the same time, there are studies that indicate a significant increase in ferritin in patients with disseminated tuberculosis relative to other clinical forms. Currently, the incidence of tuberculosis in patients with HIV infection is increasing, while diagnostic tests are not very informative. The search for diagnostic markers in terms of iron metabolism may open up new possibilities for the diagnosis of pulmonary tuberculosis.

scholarly journals Enhancement of iron toxicity in L929 cells by d-glucose: accelerated(re-)reduction

2002 ◽  
Vol 368 (2) ◽  
pp. 517-526 ◽  
Author(s):  
Ilka LEHNEN-BEYEL ◽  
Herbert de GROOT ◽  
Ursula RAUEN
Keyword(s):  
Ethyl Ester ◽  
Iron Reduction ◽  
Cell Damage ◽  
Reduction Rate ◽  
Fold Increase ◽  
Iron Complex ◽  
Iron Toxicity ◽  
Intracellular Iron ◽  
Iron Valence ◽  
Iron Pool

It has recently been shown that an increase in the cellular chelatable iron pool is sufficient to cause cell damage. To further characterize this kind of injury, we artificially enhanced the chelatable iron pool in L929 mouse fibroblasts using the highly membrane-permeable complex Fe(III)/8-hydroxyquinoline. This iron complex induced a significant oxygen-dependent loss of viability during an incubation period of 5h. Surprisingly, the addition of d-glucose strongly enhanced this toxicity whereas no such effect was exerted by l-glucose and 2-deoxyglucose. The assumption that this increase in toxicity might be due to an enhanced availability of reducing equivalents formed during the metabolism of d-glucose was supported by NAD(P)H measurements which showed a 1.5—2-fold increase in the cellular NAD(P)H content upon addition of d-glucose. To assess the influence of this enhanced cellular reducing capacity on iron valence we established a new method to measure the reduction rate of iron based on the fluorescent iron(II) indicator PhenGreen SK. We could show that the rate of intracellular iron reduction was more than doubled in the presence of d-glucose. A similar acceleration was achieved by adding the reducing agents ascorbate and glutathione (the latter as membrane-permeable ethyl ester). Glutathione ethyl ester, as well as the thiol reagent N-acetylcysteine, also caused a toxicity increase comparable with d-glucose. These results suggest an enhancement of iron toxicity by d-glucose via an accelerated (re-)reduction of iron with NAD(P)H serving as central electron provider and ascorbate, glutathione or possibly NAD(P)H itself as final reducing agent.

Physiological significance and needs of schoolchildren for nutrients

2021 ◽  
pp. 132-137
Author(s):  
O.V. Evdokimova ◽  
T.N. Ivanova ◽  
E.A. Alfimova
Keyword(s):  
Physiological Significance

The problems of non-rational nutrition of schoolchildren and the associated consequences are substantiated, the role of individual nutrients in the processes of growth and formation of the child's body is indicated, the norms of the physiological need for basic nutrients, vitamins and minerals for schoolchildren of different age categories are provided, and the ways of solving the problem are suggested.

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