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Willows (Salix spp.) are characterized by having large biomass, high tolerance to flooding, and strong metal accumulation ability, exhibiting great promise in the phytoremediation of iron (Fe) from contaminated sites. In this study, the variation of Fe tolerance and accumulation in 24 willow clones was investigated with two levels of Fe(II)-EDTA, 0.025 mM (control) and 2.0 mM (treatment) by hydroponic system for 21 days in a greenhouse. Visual symptoms of Fe toxicity were observed in the leaves and roots of Fe sensitive clones. Clonal comparisons showed a great variation in Fe tolerance, and the high levels of Fe reduced biomass productions of most clones. Tolerance indexes (TIs) varied about five-fold based on shoot dry biomass and about six-fold based on root dry biomass among clones. Clones also exhibited a wide variation in Fe concentrations (mg g-1 DW), ranged from 0.80 to 3.41 in leaves, from 5.40 to 10.51 in stems, and from 3.25 to 17.10 in roots under Fe treatments among clones. Large differences varied in the transport of Fe from roots to aerial parts among clones. The results highlighted the selection of Salix clones with high resistance to Fe toxicity and high Fe accumulation to improve phytoremediation efficacy. [ABSTRACT FROM AUTHOR]

Highlights • In 2008 Canadian guidelines on management of iron overload (IOL) in MDS were published. • Canadian hematologists with an interest in MDS here update the IOL guidelines. • Evidence for toxicity of IOL and clinical benefit of iron reduction are reviewed. • Evidence levels and recommendation grading are provided for all clinical endpoints. • Clinical management of IOL; who, when, why and how to treat IOL in MDS are addressed. Abstract In 2008 the first evidence-based Canadian consensus guideline addressing the diagnosis, monitoring and management of transfusional iron overload in patients with myelodysplastic syndromes (MDS) was published. The Canadian Consortium on MDS, comprised of hematologists from across Canada with a clinical and academic interest in MDS, reconvened to update these guidelines. A literature search was updated in 2017; topics reviewed include mechanisms of iron overload induced cellular damage, evidence for clinical endpoints impacted by iron overload including organ dysfunction, infections, marrow failure, overall survival, acute myeloid leukemia progression, and endpoints around hematopoietic stem-cell transplant. Evidence for an impact of iron reduction on the same endpoints is discussed, guidelines are updated, and areas identified where evidence is suboptimal. The guidelines address common questions around the diagnosis, workup and management of iron overload in clinical practice, and take the approach of who, when, why and how to treat iron overload in MDS. Practical recommendations for treatment and monitoring are made. Evidence levels and grading of recommendations are provided for all clinical endpoints examined. [ABSTRACT FROM AUTHOR]

In constructed wetlands (CWs) with forced aeration and vertical flow, plants can suffer from iron (Fe) deficiency due to Fe immobilization in the gravel substrate as a consequence of the oxic condition. The common reed ( Phragmites australis ) is the most commonly used plant species in CWs and frequently displays Fe-deficiency symptoms particularly in new-established systems. The aim of this study was therefore to study the Fe-nutrition of P. australis in order to gain knowledge on how Fe-deficiency in P. australis can be alleviated. For this purpose, we grew two genetically distinct phylogeographic groups of P. australis hydroponically with seven different Fe concentrations (0, 0.1, 0.2, 0.5, 1.0, 5.0 and 20.0 mg Fe-EDDHA ([iron (3+) ethylenediamine di (o-hydroxyphenylacetic) acid]) L −1 ) in a phytotron. Both groups responded strongly to the increasing Fe supply. The belowground biomass allocation ratio, light-saturated photosynthesis rates, chlorophyll content and leaf Fe tissue concentration all significantly increased with increasing Fe availability. Phragmites australis in the 0 mg Fe-EDDHA L −1 treatment suffered strongly from Fe deficiency, and plants in the high 20.0 mg Fe-EDDHA L −1 treatment also had reduced growth and Fe toxicity symptoms. The ‘critical deficiency concentration’ of Fe in leaves of juvenile P. australis was 40–50 mg kg −1 DM, and the ‘critical toxicity concentration’ of Fe in leaves of juvenile P. australis were approximately 150 mg kg −1 DM. Overall the two genetically distinct P. australis groups differed in their ecophysiological traits, and the two groups also responded differently to the different Fe-supply rates which may be the result of adaptations obtained in their native growth habitats. We suggest that the Fe-deficiency in CW systems with unsaturated vertical flow and/or forced aeration can be alleviated by application of a foliar spray containing chelated iron. However, the application rate and frequency should be further studied. [ABSTRACT FROM AUTHOR]

Iron is an absolute requirement for both the host and most pathogens alike and is needed for normal cellular growth. The acquisition of iron by biological systems is regulated to circumvent toxicity of iron overload, as well as the growth deficits imposed by iron deficiency. In addition, hosts, such as humans, need to limit the availability of iron to pathogens. However, opportunistic pathogens such as Candida albicans are able to adapt to extremes of iron availability, such as the iron replete environment of the gastrointestinal tract and iron deficiency during systemic infection. C. albicans has developed a complex and effective regulatory circuit for iron acquisition and storage to circumvent iron limitation within the human host. As C. albicans can form complex interactions with both commensal and pathogenic co-inhabitants, it can be speculated that iron may play an important role in these interactions. In this review, we highlight host iron regulation as well as regulation of iron homeostasis in C. albicans. In addition, the review argues for the need for further research into the role of iron in polymicrobial interactions. Lastly, the role of iron in treatment of C. albicans infection is discussed. [ABSTRACT FROM AUTHOR]

Deferoxamine (DFO) to treat iron overload (IO) has been limited by toxicity issues and short circulation times and it would be desirable to prolong circulation to improve non-transferrin bound iron (NTBI) chelation. In addition, DFO is currently unable to efficiently target the large pool of iron in the liver and spleen. Nanogel-Deferoxamine conjugates (NG-DFO) can prove useful as a model to investigate the pharmacokinetic (PK) properties and biodistribution (BD) behavior of iron-chelating macromolecules and their overall effect on serum ferritin levels. NG-DFO reduced the cytotoxicity of DFO and significantly reduced cellular ferritin levels in IO macrophages in vitro . PK/BD studies in normal rats revealed that NG-DFO displayed prolonged circulation and preferential accumulation into the liver and spleen. IO mice treated with NG1-DFO presented significantly lower levels of serum ferritin compared to DFO. Total renal and fecal elimination data point to the need to balance prolonged circulation with controlled degradation to accelerate clearance of iron-chelating macromolecules. [ABSTRACT FROM AUTHOR]

In this investigation, the crystal chemical characterization of one sample of woolly erionite-K (Lander County, NV, USA) was examined after suspension in a FeCl2 solution, in anaerobic conditions. The aim of this study was to determine the effect of the chemical composition of erionite on its efficiency to bind iron. Inductively coupled plasma (ICP) results showed that the sample bound Fe(II) through an ion-exchange mechanism mainly involving Ca. In addition, chemical and structural data indicated that Fe(II) is fixed at the Ca3 site, six-fold coordinated to water molecules. According to Brunauer--Emmett--Teller (BET) sample surface area the amount of Fe(II) bound by the fibers was comparable with that retrieved for fibrous erionite-Na sample from Rome (OR, USA) for which the ion-exchange process mainly affected Na. This finding provides clear evidence of a strong tendency of Fe(II) to bind to the erionite structure. Furthermore, considering that the woolly erionite-K from Langer County differs markedly from erionite-Na from Rome in the extra-framework cation content, our observations indicate that the Fe binding efficiency is not significantly modulated by the chemical composition. Notably, Fe ion-exchanged and/or accumulated on the fiber surface can generate hydroxyl radicals via the Fenton reaction, thus influencing the potential carcinogenicity of the different erionite species. [ABSTRACT FROM AUTHOR]

The mechanisms of growth inhibition and antioxidative response were investigated in wheat roots exposed to 300 μM iron together with different zinc concentrations (0, 50, and 250 μM). All Zn concentrations decreased Fe content but increased Zn content in the roots and leaves of Fe-treated seedlings. Compared with Fe stress alone, 50 or 250 μM Zn + Fe treatment stimulated root growth, and increased cell viability but decreased malondialdehyde content, which were correlated with the decreases of total and apoplastic hydrogen peroxide and superoxide anion radical (O ) content along with apoplastic hydroxyl radical content. Generation of O in response to 10 μM diphenylene iodonium suggested that NADPH oxidase activity was lower in Zn + Fe-treated roots than in other roots. In addition, cell wallbound peroxidase, diamine oxidase, and polyamine oxidase in Fe-treated roots were insensitive to Zn addition. Further study showed the stimulation of total superoxide dismutase and glutathione reductase (GR) activities as well as apoplastic catalase, ascorbate peroxidase, and GR in Zn + Fe-stressed roots in comparison with Fe-alone-treated ones. Taken together, Zn could alleviate iron-inhibitory effect on root growth, which might be associated with the decrease of lipid peroxidation, the increase of cell viability and the reductions of reactive oxygen species generation. [ABSTRACT FROM AUTHOR]

The toxicological effects of FeO nanoparticles were evaluated with an iron-corroding bacterium (ICB) for preventing the biocorrosion of iron. FeO nanoparticles of 18 nm were successfully prepared and characterized by transmission electron microscopy (TEM), X-ray diffraction (XRD) patterns and scanning electron microscopy-energy dispersive X-ray spectroscopy (SEM-EDS). A halophilic ICB strain L4 was isolated from Ribandar saltpan Goa, India and identified biochemically and by 16S rRNA gene sequence analysis as Halanaerobium sp. The FeO nanoparticles in increasing doses (0.1-100 mg/L) caused transformation in growth and sulfide production of ICB strain L4. SEM-EDS analysis revealed a deformed cell structure with adsorption of nanoparticle on the cell surface and increased cell size. Comet assay revealed genotoxic effect of FeO nanoparticles on strain L4 which resulted in dose-dependent DNA damage by increasing percentage tail DNA from 5 to 88% with increasing FeO nanoparticles concentration. Furthermore, sulfide production rate was reduced to 11.8% in presence of 100 mg/L FeO nanoparticles which reduced the corroding property of ICB strain L4; thus, it was unable to corrode the iron nail in presence of FeO nanoparticle. This work suggests the possible application of FeO nanoparticle in addressing biocorrosion problems faced by different industries. [ABSTRACT FROM AUTHOR]

Thallium (Tl) is highly toxic to mammals and relevant pollution cases are increasing world-widely. Convenient and efficient method for the removal of trace Tl from contaminated source water is imperative. Here, the removal of trace Tl by K 2 FeO 4 [Fe(VI)] was investigated for the first time, with the exploration of reaction mechanisms. Six different types of water treatment agents (powdered activated carbon, Al 2 (SO 4 ) 3 , FeCl 3 , δ-MnO 2 , MnO 2 nano-particles, and K 2 FeO 4 ) were used for the removal of Tl in spiked river water, and K 2 FeO 4 showed excellent removal performance. Over 92% of Tl (1 μg/L) was removed within 5 min by applying 2.5 mg/L of K 2 FeO 4 (pH 7.0, 20 °C). XPS analysis revealed that in the reaction of Tl(I) with K 2 FeO 4 , Tl(I) was oxidized to Tl(III), and removed by the K 2 FeO 4 reduced ferric particles. The removal of Tl by in situ formed and ex situ formed ferric particle was examined respectively, and the results revealed that the removal of trace Tl could be attributed to the combination of adsorption and coprecipitation processes. The hydrodynamic size of the reduced particle from K 2 FeO 4 ranged from 10 nm to 100 nm, and its surface was negatively charged under neutral pH condition. These factors were conducive for the efficient removal of Tl by K 2 FeO 4 . The effects of solution pH, coexisting ions (Na + , Ca 2+ , and HCO 3 − ), humic acid, solution temperature, and reductive environment on the removal and desorption of Tl were investigated, and the elimination of Tl in polluted river water and reservoir water was performed. These results suggest that K 2 FeO 4 could be an efficient and convenient agent on trace Tl removal. [ABSTRACT FROM AUTHOR]

P is one of the macronutrients required for plant growth and development, whereas Fe is a micronutrient required for various metabolic functions of plant. However, under acidic soil conditions, due to low pH Fe2+ toxicity and P deficiency occurs leading to decrease in crop productivity. The present investigation was undertaken to understand molecular physiology of acidity tolerance with special reference to P-deficiency and Fe-toxicity tolerance in Shasarang (LR11). Under lowland acid soils (pH=5.2), KMR3 showed a higher bronzing score of 3 at 110 DAT and LR11 showed very little or no bronzing. The field performance of LR11 was better as compared to KMR3 with respect to yield related traits. Furthermore, our data confirmed that LR11 is infact Fe toxicity tolerant and "Shasarang" means "tolerant to Fe" in Khasi. The susceptible genotype, KMR3, showed significant decrease in shoot and root dry weight under low P and Fe toxicity conditions in hydroponic. However, in LR11, the difference in root-shoot dry weight in control and treatment were not significant. Excess amounts of iron in hydroponics could lead to distinct variation in the bronzing score, root-shoot biomass. Based on this criteria Nipponbare has been considered tolerant and Kasalath as susceptible. In our case, screening using excess of Fe and low P simultaneously, Kasalath performed at par with LR11. This study, therefore, suggests that identified tolerant LR11 can be a potential target for enhancing rice production introducing tolerance to acidity under lowland rainfed field conditions. [ABSTRACT FROM AUTHOR]

Background: Ferrous iron (Fe) and zinc (Zn) at high concentration in the soil cause heavy metal toxicity and greatly affect rice yield and quality. To improve rice production, understanding the genetic and molecular resistance mechanisms to excess Fe and Zn in rice is essential. Genome-wide association study (GWAS) is an effective way to identify loci and favorable alleles governing Fe and Zn toxicty as well as dissect the genetic relationship between them in a genetically diverse population. Results: A total of 29 and 31 putative QTL affecting shoot height (SH), root length (RL), shoot fresh weight (SFW), shoot dry weight (SDW), root dry weight (RDW), shoot water content (SWC) and shoot ion concentrations (SFe or SZn) were identified at seedling stage in Fe and Zn experiments, respectively. Five toxicity tolerance QTL (qSdw3a, qSdw3b, qSdw12 and qSFe5 / qSZn5) were detected in the same genomic regions under the two stress conditions and 22 candidate genes for 10 important QTL regions were also determined by haplotype analyses. Conclusion: Rice plants share partial genetic overlaps of Fe and Zn toxicity tolerance at seedling stage. Candidate genes putatively affecting Fe and Zn toxicity tolerance identified in this study provide valuable information for future functional characterization and improvement of rice tolerance to Fe and Zn toxicity by marker-assisted selection or designed QTL pyramiding. [ABSTRACT FROM AUTHOR]

Oxygen is essential for aerobic organisms but causes cytotoxicity probably through the generation of reactive oxygen species (ROS). In this study, we screened for the genes that regulate oxidative stress in the yeast Saccharomyces cerevisiae, and found that expression of CTH2/ TIS11 caused an increased resistance to ROS. CTH2 is up-regulated upon iron starvation and functions to remodel metabolism to adapt to iron starvation. We showed here that increased resistance to ROS by CTH2 would likely be caused by the decreased ROS production due to the decreased activity of mitochondrial respiration, which observation is consistent with the fact that CTH2 down-regulates the mitochondrial respiratory proteins. We also found that expression of CTH1, a paralog of CTH2, also caused an increased resistance to ROS. This finding supported the above view, because mitochondrial respiratory proteins are the common targets of CTH1 and CTH2. We further showed that supplementation of iron in medium augmented the growth of S. cerevisiae under oxidative stress, and expression of CTH2 and supplementation of iron collectively enhanced its growth under oxidative stress. Since CTH2 is regulated by iron, these findings suggested that iron played crucial roles in the regulation of oxidative stress in S. cerevisiae. [ABSTRACT FROM AUTHOR]

The budding yeast Saccharomyces cerevisiae stores iron in the vacuole, which is a major resistance mechanism against iron toxicity. One key protein involved in vacuolar iron storage is the iron importer Ccc1, which facilitates iron entry into the vacuole. Transcription of the CCC1 gene is largely regulated by the binding of iron-sulfur clusters to the activator domain of the transcriptional activator Yap5. Additional evidence, however, suggests that Yap5-independent transcriptional activation of CCC1 also contributes to iron resistance. Here, we demonstrate that components of the signaling pathway involving the low-glucose sensor Snf1 regulate CCC1 transcription and iron resistance. We found that SNF1 deletion acts synergistically with YAP5 deletion to regulate CCC1 transcription and iron resistance. A kinase-dead mutation of Snf1 lowered iron resistance as did deletion of SNF4, which encodes a partner protein of Snf1. Deletion of all three alternative partners of Snf1 encoded by SIT1, SIT2, and GAL83 decreased both CCC1 transcription and iron resistance. The Snf1 complex is known to activate the general stress transcription factors Msn2 and Msn4. We show that Msn2 and Msn4 contribute to Snf1-mediated CCC1 transcription. Of note, SNF1 deletion in combination with MSN2 and MSN4 deletion resulted in additive effects on CCC1 transcription, suggesting that other activators contribute to the regulation of CCC1 transcription. In conclusion, we show that yeast have developed multiple transcriptional mechanisms to regulate Ccc1 expression and to protect against high cytosolic iron toxicity. [ABSTRACT FROM AUTHOR]

Although iron is necessary for brain tissue, its overload causes many metabolic disorders as well as neurodegenerative disorders. Syntaxin4 and synapsin3 are proteins associated with synaptic vesicles that play a role in neurotransmitter release. In this study we investigated the effects of sublethal doses of ferric iron at 0.87 ppm, 3 ppm, 30 ppm and 300 ppm on mRNA levels of genes coding syntaxin4 and synapsin3 proteins that function in nerve cell signal transmission in cortex and hippocampus tissues of rats (Rattus norvegicus). While mRNA level of the syntaxin4 gene was unchanged in the cortex, mRNA level of syntaxin4 decreased with 30 ppm and 300 ppm exposure in the hippocampus. mRNA level of synapsin3 gene in both cortex and hippocampus tissues increased in all treatment groups compared to control group. [ABSTRACT FROM AUTHOR]

The selection of plant species resistant to iron toxicity is important in the ecological rehabilitation of mining areas. The objective of our study was to identify the degree of resistance of the grasses Paspalum densum, Hyparrhenia rufa, and Echinochloa crus-galli to iron toxicity on the basis of physiological and biochemical responses in a nutrient solution. The experiments initially consisted of hydroponic cultivation of the three plant species to evaluate short-term responses at increasing concentrations of Fe-EDTA 0.009 (control), 1, 2, 4, 7, and 9 mM; and afterward by prolonged exposure of the resistant grasses to Fe-EDTA concentrations of 0.009 and 7 mM. Iron concentration increased in the leaves of all species evaluated, showing values above the phytotoxic threshold. P. densum and E. crus-galli were selected in view of their resistance to iron toxicity, evidenced mainly by low malondialdehyde (MDA) values due to mechanisms of tolerance and avoidance. In contrast, H. rufa showed an increase in MDA values and a reduction in gas exchange, revealing considerable sensitivity to iron toxicity. The results showed the potential for using P. densum and E. crus-galli in the revegetation of areas degraded by mining iron. [ABSTRACT FROM AUTHOR]

This study investigated the concentration of potentially toxic elements (PTEs) including Al, As, Cd, Co, Cr, Cu, Fe, Hg, Mn, Mo, Ni, Pb, Sb, V, and Zn in 102 soils (in the Near and Far areas of the mine), 7 tailings, and 60 plant samples (shoots and roots of Artemisia sieberi and Zygophylum species) collected at the Gol-E-Gohar iron ore mine in Iran. The elemental concentrations in tailings and soil samples (in Near and Far areas) varied between 7.4 and 35.8 mg kg for As (with a mean of 25.39 mg kg for tailings), 7.9 and 261.5 mg kg (mean 189.83 mg kg for tailings) for Co, 17.7 and 885.03 mg kg (mean 472.77 mg kg for tailings) for Cu, 12,500 and 400,000 mg kg (mean 120,642.86 mg kg for tailings) for Fe, and 28.1 and 278.1 mg kg (mean 150.29 mg kg for tailings) for Ni. A number of physicochemical parameters and pollution index for soils were determined around the mine. Sequential extractions of tailings and soil samples indicated that Fe, Cr, and Co were the least mobile and that Mn, Zn, Cu, and As were potentially available for plants uptake. Similar to soil, the concentration of Al, As, Co, Cr, Cu, Fe, Mn, Mo, Ni, and Zn in plant samples decreased with the distance from the mining/processing areas. Data on plants showed that metal concentrations in shoots usually exceeded those in roots and varied significantly between the two investigated species ( Artemisia sieberi > Z ygophylum). All the reported results suggest that the soil and plants near the iron ore mine are contaminated with PTEs and that they can be potentially dispersed in the environment via aerosol transport and deposition. [ABSTRACT FROM AUTHOR]

The regulation of iron metabolism in biological systems centers on providing adequate iron for cellular function while limiting iron toxicity. Because mammals cannot excrete iron, mechanisms have evolved to control iron acquisition, storage, and distribution at both systemic and cellular levels. Hepcidin, the master regulator of iron homeostasis, controls iron flows into plasma through inhibition of the only known mammalian cellular iron exporter ferroportin. Hepcidin is feedback-regulated by iron status and strongly modulated by inflammation and erythropoietic demand. This review highlights recent advances that have changed our understanding of iron metabolism and its regulation. [ABSTRACT FROM AUTHOR]

This study was designed to evaluate how varicocele ( VCL) can time dependently induce zinc (Zn) and iron (Fe) toxicity in testicular tissue and to analyse the relation between heavy metals toxicity and lipid peroxidation, sperm DNA damage, nitrosative and carbonyl stresses. Twenty-four mature male Wistar rats were divided into control-sham and test groups, which were then submitted to experimentally induced VCL. Non- VCL-induced rats were considered as control-sham. The test groups were subdivided into three groups based on the sample collecting date (2, 6 and 8 months after VCL induction). Zn and Fe distribution in testicles, DNA ladder for sperm DNA fragmentation, testicular total antioxidant capacity ( TAC), malondialdehyde ( MDA), nitrite oxide ( NO) and carbonyl groups ( CG) were analysed. A significant ( p < .05) enhancement in the percentage of tubules with negative tubular repopulation, differentiation and spermiogenesis indices was revealed. The VCL increased Zn and Fe distribution in testicles. The VCL, time dependently, reduced sperm count, motility and enhanced sperm DNA damage ( p < .05). The VCL downregulated the testicular TAC and enhanced the MDA, NO and CG contents. Our data showed that the VCL results in intensive Fe and Zn toxicities. Produced Zn- and Fe-mediated-oxidative stress increases sperm DNA damage associated with NO and CG-induced stresses. [ABSTRACT FROM AUTHOR]

Background and aims: Understanding the potential effects of iron toxicity on plant development is important when constructing new wetland from iron-rich sediment. We aim to study plant species-specific effects of iron toxicity when grown in the iron-rich sediments of lake Markermeer (the Netherlands). Methods: Using three sediment sources that varied in total Fe and Fe-P concentrations, we performed a greenhouse experiment to study the development of three wetland species that differ in their tolerance to iron and utilization capacity of Fe-P: Rumex maritimus, Phragmites australis and Eupatorium cannabinum. Results: Phragmites australis was the only species that developed an epidermis-damaging iron plaque on its roots. Plaque formation mainly depended on the Fe(III) and Fe-P concentration of the sediment, which led to different nutrient imbalances in leaves. All three species showed reduced growth compared to the control substrate, which could not be linked to indirect Fe toxicity. In contrast, direct Fe toxicity following the uptake of Fe could not be excluded as a mechanism potentially explaining our results, and this result warrants further examination in longer-term experiments. Conclusions: Our results highlight the importance of considering the Fe and Fe-P availability in sediments, as these properties may constrain plant performance and delay the development of pioneer ecosystems in wetland construction sites. [ABSTRACT FROM AUTHOR]

This study reports a series of experiments conducted to evaluate the suitability of thiourea dioxide (TD) under mechanical activation, in bleaching iron-bearing impurities from raw kaolin. The optimum conditions for the maximum whiteness of 76.32% were determined as follows: rotation speed of ball mill, 400 rpm; activation time, 1.5 h; TD dosage, 0.8% of kaolin mass; solid-to-liquid ratio, 1:2; pH, 8.0; room temperature. The effect of grinding causes the partial surface amorphization of kaolin particles and a decrease in the dehydroxylation temperature. The assistance of grinding leads to a higher iron removal when compared with the conventional bleaching method using sodium hydrosulfite. [ABSTRACT FROM AUTHOR]

Unsaturated incubation (UI) of air-dried soil before flooding significantly reduced the reduction of redox potential and decreased the easily reducible iron (Fe) (ERFe). Antibacterial treatment of the soil decreased the ERFe level regardless of the moisture regime while fungicide treatment reduced the effects of UI. Treating soil under imposed UI with sucrose helped recover the ERFe to the non-UI level. The effects of UI disappeared after air-drying the soil; therefore, the decrease in ERFe—by imposing upland conditions before flooding—could be due to the decrease in the activity of iron-reducing bacteria owing to the depletion of respiratory substrates by bacterial activity during the upland conditions. These results indicate that a drastic change in soil moisture from dry to wet will increase the risk of iron toxicity by increasing the ERFe, but that maintaining an upland condition for more than one week before total submergence can reduce the risk of iron toxicity. [ABSTRACT FROM PUBLISHER]

Iron is an essential micronutrient that is problematic for biological systems since it is toxic as it generates free radicals by interconverting between ferrous (Fe 2 + ) and ferric (Fe 3 + ) forms. Additionally, even though iron is abundant, it is largely insoluble so cells must treat biologically available iron as a valuable commodity. Thus elaborate mechanisms have evolved to absorb, re-cycle and store iron while minimizing toxicity. Focusing on rarely encountered situations, most of the existing literature suggests that iron toxicity is common. A more nuanced examination clearly demonstrates that existing regulatory processes are more than adequate to limit the toxicity of iron even in response to iron overload. Only under pathological or artificially harsh situations of exposure to excess iron does it become problematic. Here we review iron metabolism and its toxicity as well as the literature demonstrating that intracellular iron is not toxic but a stress responsive programmed cell death-inducing second messenger. [ABSTRACT FROM AUTHOR]

Though toxic in excess, iron is vital for life. Thus, its use in all cells is tightly regulated. Analysis of Saccharomyces cerevisiae, which has been used extensively as a model system, has revealed layers of regulation of cellular iron trafficking and utilization. This regulation is based on the availability of both elemental iron and functionality of the Fe-S cluster biogenesis system. Here, we discuss a possible 'first responder' regulatory mechanism centered on the stability of the scaffold protein on which Fe-S clusters are built. [ABSTRACT FROM AUTHOR]

Magnetic microparticles (MPs) have been recently proposed as a new and promising tool for restoring eutrophicated waters. In this study, we analyzed the acute (immobilization) and chronic effects of iron (Fe) MPs on Daphnia magna and on the benthic macroinvertebrate Chironomus sp. In the chronic toxicity tests the offspring production (male and female) in D. magna and the mortality of larvae and pupae, and adult emergence in Chironomus sp. experiments were used as the endpoints. The concentration of MPs that caused 50% of immobilized individuals (EC 50 ) in the acute toxicity test was much higher in D. magna (0.913 g MPs l −1 ) than in Chironomus sp. (0.445 g MPs l −1 ). The results of chronic toxicity tests in D. magna showed that in presence of dissolved Fe (dFe), parthenogenetic reproduction was significantly affected, while no significant effect on mortality of larvae and pupae and on adult emergence was detected in Chironomus sp. test. Taking into account both that long-term exposure is not likely to occur and the regular dose of MPs potentially used in a restoration plan, we conclude that MPs is a riskless (no toxic effect on planktonic and benthic organisms) and efficient (high P adsorption capacity) tool for lake restoration. [ABSTRACT FROM AUTHOR]

Acute iron intoxication (FeI) in humans has not been adequately studied. The manifestation of FeI, defined as a serum iron concentration >300 µg/dL (55 µmol/L) within 12 hours of ingestion, include various symptoms appearing in progressive stages. Systemic toxicity is expected with an intake of 60 mg/kg. A 27-year-old female nurse presented with unintended acute intravenous iron intoxication (FeI) a week after self-injecting herself with 20 ampoules of IV iron (4,000 mg elemental iron, 60 mg/kg). She had stable vital signs and mild hepatic tenderness. Hepatic MRI (Ferriscan®) showed a moderate/severe liver iron content (LIC: 9 mg/g dry tissue). Her hemogram, electrolytes, hepatic and renal functions were normal. Based on the high dose of iron received and her elevated LIC, chelation therapy was advised. She accepted only oral therapy and was started on deferasirox at a dose of 30 mg /kg daily. This oral chelation proved to be effective in clearing her hepatic iron overload after six months (LIC: 2 mg /g dry tissue), without side effects. This case also proved the value of Ferriscan® in diagnosing the degree of hepatic FeI and monitoring therapy to achieve a safe level of LIC. [ABSTRACT FROM AUTHOR]

Deferoxamine (DFO), an iron chelator, is commonly used to remove excess iron from the body. DFO has also been demonstrated to have anti-tumor effect. However, there is no available report on the effect of deferoxamine on mesenchymal stromal cells (MSCs). In this study, we first isolated tumor-associated MSCs (TAMSCs) from EG-7 tumors, which were positive for CD29, CD44, CD73, CD90 and CD105. Ex vivo cultured stem cells derived from tumor and bone marrow compartment were exposed to DFO. We demonstrated that DFO had growth-arresting and apoptosis-inducing effect on TAMSCs and bone marrow MSCs (BMMSCs). DFO also influenced the expression pattern of adhesion molecule VCAM-1 on both TAMSCs and BMMSCs. Notwithstanding its widespread use, our results here warrants caution in the application of DFO, and also highlights the need for careful evaluation of the bone marrow compartment in patients receiving DFO treatment. [ABSTRACT FROM AUTHOR]

The effectiveness of rice germplasm utilization in breeding programs for improving iron toxicity tolerance requires an understanding of their genetics mode. Here, we study estimating gene effect using digital imaging method for iron toxicity tolerance in rice seedling. The proportion of intensity of color red (R)/green (G) index was analyzed by Adobe Photoshop CS3©. Validation was done using 23 genotypes of rice seedling under 400 mg.L-1 Fe 2+ using Yoshida-agar solution. A genetics study was done using the six-generation population of 2 crosses between 2 iron toxicity tolerant varieties with an iron-toxicity sensitive variety (Inpara 5 x Mahsuri and Inpara 5 x Pokkali). The seedlings of parents and their progeny were phenotyped under same iron concentration for screening above. The simple additive-dominance which did not fit to the model indicated the presence of non-allelic gene interactions or epistasis in all observed traits. Five parameter models, additive x additive (i), additive x dominance (j) and dominance x dominance (l) epistasis, in addition to additive (d) and dominance (h) were fit for gene action explanation of the observed traits in both populations. These type of gene actions were duplicate epistasis in both crosses, except for R/G in cross of Inpara 5/Pokkali. R/G index showed strong correlation with LBS, shoot length, and root length in the F2 population. Estimated broad and narrow-sense heritability of observed traits were medium to high and medium to low, respectively. [ABSTRACT FROM AUTHOR]

An excessive amount of iron may become extremely toxic both for its ability to generate reactive oxygen species, and for the lack of regulatory mechanisms for iron excretion in humans. Chelation therapy has been introduced in clinical practice in the 1970′s to defend thalassemia patients from the effects of iron overload and it has dramatically changed both life expectancy and quality of life. The disadvantages of the drugs in clinical use make the research for new, more suitable iron chelating agents, urgent. This review defines the requirements of an iron chelator, then points out the principal chemical features of the iron chelators in use. Finally, a survey on the last ten years of the literature relative to iron chelators is done, and the most interesting ligands are presented, with particular emphasis to those that reached clinical trials. [ABSTRACT FROM AUTHOR]

Excess iron (Fe) is phytotoxic and causes reduced growth and productivity in rice. In this study we elucidated the mechanisms conferring differential tolerance to Fe-toxicity in rice seedlings. Excess Fe caused retardation in roots of both Pokkali and BRRI 51, but it caused no significant changes on growth parameters, Fe accumulation and OsIRT1 expression in shoots of Pokkali only compared with control plants. These results suggest that the Pokkali genotype does have mechanisms in shoots to withstand Fe toxicity. Pokkali maintained membrane stability and total soluble protein in shoots due to Fe toxicity, further confirming its ability to tolerate excess Fe. Furthermore, a significant decrease of Fe-chelate reductase activity and OsFRO1 expression in shoots of Pokkali suggests that limiting Fe accumulation is possibly regulated by Fe-reductase activity. Our extensive expression analysis on the expression pattern of three chelators (OsDMAS1, OsYSL15, OsYSL2 and OsFRDL1) showed no significant changes in expression in shoots of Pokkali due to Fe toxicity, whereas these genes were significantly upregulated under Fe-toxicity in sensitive BRRI 51. These results imply that regulation of Fe chelation in shoots of Pokkali contributes to its tolerance to Fe toxicity. Finally, increased catalase (CAT), peroxidase (POD), glutathione reductase (GR) and superoxide dismutase (SOD), along with elevated ascorbic acid, glutathione, cysteine, methionine and proline in shoots of Pokkali caused by Fe toxicity suggests that strong antioxidant defence protects rice plants from oxidative injury under Fe toxicity. Taking these results together, we propose that genetic variation in Fe-toxicity tolerance in rice is shoot based, and is mainly associated with the regulation of translocation and chelation of Fe together with elevated antioxidant metabolites in shoots. [ABSTRACT FROM AUTHOR]

With the increasing environmental application and discharge of iron-based nanoparticles (NPs), a comprehensive understanding of their fate and ecotoxicological effect in the aquatic environment is very urgent. In this study, toxicities of 4 zero-valent iron NPs (nZVI) of different sizes, 2 Fe 2 O 3 NPs of different crystal phases, and 1 type of Fe 3 O 4 NPs to a green alga ( Chlorella pyrenoidosa ) were investigated, with a focus on the effects of particle size, crystal phase, oxidation state, and environmental aging. Results show that the algal growth inhibition of nZVI increased significantly with decreasing particle size; with similar particle sizes (20–30 nm), the algal growth inhibition decreased with oxidation of the NPs with an order of nZVI > Fe 3 O 4 NPs > Fe 2 O 3 NPs, and α-Fe 2 O 3 NPs presented significantly higher toxicity than γ-Fe 2 O 3 NPs. The NP-induced oxidative stress was the main toxic mechanism, which could explain the difference in algal toxicity of the NPs. The NP-cell heteroagglomeration and physical interactions also contributed to the nanotoxicity, whereas the effect of NP dissolution was negligible. The aging in distilled water and 3 surface water samples for 3 months increased surface oxidation of the iron-based NPs especially nZVI, which decreased the toxicity to algae. These findings will be helpful for the understanding of the fate and toxicity of iron-based NPs in the aquatic environment. [ABSTRACT FROM AUTHOR]

The objective of this study was to assess the reliability of pot-based screening method for iron (Fe) toxicity tolerance in rice using soils from hot spots. Five lowland rice varieties with known reaction to Fe toxicity were grown in pots in a screen house for three seasons. Fe-toxic soils from two hot spot fields – Edozighi, Nigeria and Niaouli, Benin were used and soil from Africa Rice Center (AfricaRice) experimental farm, Cotonou, Benin was included as control. Leaf bronzing score (LBS) was determined at different stages, and grain yield was determined at maturity. Heritability was estimated using data across the three seasons. High heritability was recorded for LBS and grain yield. Grain yield reduction in stress treatment relative to control varied from 15 to 56% depending on the variety and soil. Bao Thai, Suakoko 8, and WITA 4 had better performance under Fe toxicity in terms of LBS, yield and relative yield reduction, whereas Bouake 189 and IR64 had poorer performance. Grain yield and LBS were significantly correlated but negatively at 60 days after sowing (DAS). Overall, the results found in this experiment were consistent with previous field studies. Therefore, pot screening using soils from hot spots can be used by rice breeding programs to reliably assess Fe toxicity toleranceex situ. [ABSTRACT FROM AUTHOR]

Iron toxicity is major constraint of rice production in irrigated-lowland. The Improvement of tolerant rice cultivar to iron toxicity requires the information of some genetics parameters related to selected characters. This study was aimed to estimate gene action and heritability of the grain yield and its component under iron-toxic stress and control field conditions in rice. The iron-toxic tolerant rice cultivars, Pokkali and Mahsuri were crossed with the sensitive cultivar, Inpara5 to develop six generation populations. The breeding materials were grown in the iron toxicity site and control in Taman Bogo, Lampung Indonesia in the wet season from December 2013 to March 2014. The sensitive parent and BC1P1 had lower stress tolerance index (STI) compared to the tolerant parent F1, F2 and BC1P2. The grain yield and its component were fitted to the best model in five parameters which were more prominent with interactive epistasis of duplicate and complementary gene action. The heritability's under control were more higher compared to iron toxicity stress condition. Delaying selection to later generations and combining with the shuttle breeding between stressed and controlled environments were the best strategy for improving the grain yield and tolerance to iron toxicity in rice. [ABSTRACT FROM AUTHOR]

Iron intoxication is related to reactive oxygen species (ROS) production and organic damage including the cardiovascular system, and is a leading cause of poisoning deaths in children. In this study we examined whether a range of ferrous iron (Fe(2 +)) concentrations can interfere differently on the myocardial mechanics, investigating the ROS-mediated effects. Developed force of isolated rat papillary muscles was depressed with a concentration- and time-dependency by Fe(2 +) 100–1000 μM. The contractile response to Ca(2 +) was reduced, but it was partially reversed by co-incubation with catalase and DMSO, but not TEMPOL. In agreement, in situ detection of OH was increased by Fe(2 +) whereas O 2 − was unchanged. The myosin-ATPase activity was significantly decreased. Contractions dependent on the sarcolemal Ca(2 +) influx were impaired only by Fe(2 +) 1000 μM, and antioxidants had no effect. In skinned fibers, Fe(2 +) reduced the pCa-force relationship, and pCa50 was right-shifted by 0.55. In conclusion, iron overload can acutely impair myocardial contractility by reducing myosin-ATPase activity and myofibrillar Ca(2 +) sensitivity. These effects are mediated by local production of OH and H 2 O 2 . Nevertheless, in a such high concentration as 1000 μM, Fe(2 +) appears to depress force also by reducing Ca(2 +) influx, probably due to a competition at Ca(2 +) channels. [ABSTRACT FROM AUTHOR]

Iron toxicity is a nutrient disorder that severely affects crop development and yield in some soil conditions. Vacuolar detoxification of metal stress is an important strategy for plants to survive and adapt to this adverse environment. Vacuolar iron transporter (VIT) members are involved in this process and play essential roles in iron storage and transport. In this study, we identified a rapeseed VIT gene BnMEB2 (BnaC07g30170D) homologs to Arabidopsis MEB2 (At5g24290). Transient expression analysis revealed that BnMEB2 was localized to the vacuolar membrane. Q-PCR detection showed a high expression of BnMEB2 in mature (60-day-old) leaves and could be obviously induced by exogenous iron stress in both roots and leaves. Over-expressed BnMEB2 in both Arabidopsis wild type and meb2 mutant seedlings resulted in greatly improved iron tolerability with no significant changes in the expression level of other VIT genes. The mutant meb2 grew slowly and its root hair elongation was inhibited under high iron concentration condition while BnMEB2 over-expressed transgenic plants of the mutant restored the phenotypes with apparently higher iron storage in roots and dramatically increased iron content in the whole plant. Taken together, these results suggested that BnMEB2 was a VIT gene in rapeseed which was necessary for safe storage and vacuole detoxification function of excess iron to enhance the tolerance of iron toxicity. This research sheds light on a potentially new strategy for attenuating hazardous metal stress from environment and improving iron biofortification in Brassicaceae crops. [ABSTRACT FROM AUTHOR]

Renal glomerular and tubular dysfunctions have been reported with high prevalence in β-thalassemia. Iron toxicity is implicated in the kidney damage, which may be reversed by iron chelation therapy. To mimic heavy iron overload and evaluate the efficacy of iron chelators in the patients, iron dextran (180 mg iron/mouse) was intraperitoneally (i.p.) injected in heterozygous β-globin knockout mice ( muβth−3/+ , BKO) and wild type mice (C57BL/6J, WT) over a period of 2 weeks, followed by daily i.p. injection of deferoxamine (DFO) or deferiprone (L1) for 1 week. In BKO mice, iron preferentially accumulated in the proximal tubule with a grading score of 0–1 and increased to grade 3 after iron loading. In contrast, iron mainly deposited in the glomerulus and interstitial space in iron overloaded WT mice. Increased levels of kidney lipid peroxidation, glomerular and medullar damage and fibrosis in iron overloaded mice were reversed by treatment with iron chelators. L1 showed higher efficacy than DFO in reduction of glomerular iron, which was supported by a significantly decreased the amount of glomerular damage. Notably, DFO and L1 demonstrated a distinct pattern of iron distribution in the proximal tubule of BKO mice. In conclusion, chelation therapy has beneficial effects in iron-overloaded kidneys. However, the defect of kidney iron metabolism in thalassemia may be a determining factor of the treatment outcome in individual patients. [ABSTRACT FROM AUTHOR]

Fe-based nanoparticles act as new generation environmental remediation technologies, and provide cost-effective solutions to the most demanding environmental cleanup problems. Because of substantial surface area and elevated surface reactivity, Fe-based nanoparticles provide immense flexibility for in-situ applications. In recent years, zerovalent nano iron (ZVNI) and other surface modified ZVNI particles have promised the effective transformation of a wide range of common environmental toxins including chlorinated compounds, organochlorine pesticides, pharmaceuticals, polychlorinated biphenyls and other organic compounds. Surface modification of iron nanoparticles further enhances the speed and efficiency of remediation. This review encapsulated the recent reports in the remediation of environmental pollutants using various Fe-based nanoparticles. The preparation methods, characteristic properties and latest environmental applications of various Fe-based nanoparticles have been discussed in detail. Additionally, the risk assessment of different Fe-based nanoparticles and concluding remarks were described in detail followed by future perspectives to improve the efficiency of Fe-based nanoparticles towards environmental sustainability. [ABSTRACT FROM AUTHOR]

Previous studies have shown that iron redistribution and deposition in the brain occurs in some neurodegenerative diseases, and oxidative damage due to abnormal iron level is a primary cause of neuronal death. In the present study, we used the single prolonged stress (SPS) model to mimic post-traumatic stress disorder (PTSD), and examined whether iron was involved in the progression of PTSD. The anxiety-like behaviors of the SPS group were assessed by the elevated plus maze (EPM) and open field tests, and iron levels were measured by inductively coupled plasma optical emission spectrometer (ICP-OES). Expression of glucocorticoid receptors and transferrin receptor 1 (TfR1) and ferritin (Fn) was detected by Western blot and immunohistochemistry in selected brain areas; TfR1 and Fn mRNA expression were detected by quantitative-polymerase chain reaction (Q-PCR). Ultrastructures of the hippocampus were observed under a transmission electron microscope. Our results showed that SPS exposure induced anxiety-like symptoms and increased the level of serum cortisol and the concentration of iron in key brain areas such as the hippocampus, prefrontal cortex, and striatum. The stress induced region-specific changes in both protein and mRNA levels of TfR1 and Fn . Moreover, swelling mitochondria and cell apoptosis were observed in neurons in brain regions with iron accumulation. We concluded that SPS stress increased iron in some cognition-related brain regions and subsequently cause neuronal injury, indicating that the iron may function in the pathology of PTSD. [ABSTRACT FROM AUTHOR]

Iron (Fe) is essential for rice growth and humans consuming as their staple food but is often deficient because of insoluble Fe(III) in soil for rice growth and limited assimilation for human bodies, while cadmium (Cd) is non-essential and toxic for rice growth and humans if accumulating at high levels. Over-accumulated Cd can cause damage to human bodies. Selecting and breeding Fe-rich but Cd-free rice cultivars are ambitious, challenging and meaningful tasks for researchers. Although evidences show that the mechanisms of Fe/Cd uptake and accumulation in rice are common to some extent as a result of similar entry routes within rice, an increasing number of researchers have discovered distinct mechanisms between Fe/Cd uptake and accumulation in rice. This comprehensive review systematically elaborates and compares cellular mechanisms of Fe/Cd uptake and accumulation in rice, respectively. Mechanisms for maintaining Fe homeostasis and Cd detoxicification are also elucidated. Then, effects of different fertilizer management on Fe/Cd accumulation in rice are discussed. Finally, this review enumerates various approaches for reducing grain Cd accumulation and enhancing Fe content in rice. In summary, understanding of discrepant cellular mechanisms of Fe/Cd accumulation in rice provides guidance for cultivating Fe-fortified rice and has paved the way to develop rice that are tolerant to Cd stress, aiming at breeding Fe-rich but Cd-free rice. [ABSTRACT FROM AUTHOR]

Iron is an essential nutrient for every type of life on earth. However, excess iron is cytotoxic and can lead to an increased cancer risk in humans. Catalytic ferrous iron [Fe(II)] is an initiator of the Fenton reaction, which causes oxidative stress by generating hydroxyl radicals. Recently, it became possible to localize catalytic Fe(II) in situ with a turn-on fluorescent probe, RhoNox-1. Here, we screened each organ/cell of rats to globally evaluate the distribution of catalytic Fe(II) and found that eosinophils showed the highest abundance. In various cells, lysosomes were the major organelle, sharing ∼40–80% of RhoNox-1 fluorescence. We then used an ovalbumin-induced allergic peritonitis model to study the dynamics of catalytic Fe(II). Peritoneal lavage revealed that the total iron contents per cell were significantly decreased, whereas an increase in the number of inflammatory cells (macrophages, neutrophils, eosinophils and lymphocytes) resulted in an increased total iron content of the peritoneal inflammatory cells. Notably, macrophages, eosinophils and neutrophils exhibited significantly increased catalytic Fe(II) with increased DMT1 expression and decreased ferritin expression, though catalytic Fe(II) was significantly decreased in the peritoneal lavage fluid. In conclusion, catalytic Fe(II) in situ more directly reflects cellular activity and the accompanying pathology than total iron does. [ABSTRACT FROM AUTHOR]

Iron is necessary for neuronal functions; however, excessive iron accumulation caused by impairment of iron balance could damage neurons. Neuronal iron accumulation has been observed in several neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. Nevertheless, the precise mechanisms underlying iron toxicity in neuron cells are not fully understood. In this study, we investigated the mechanism underlying iron overload-induced mitochondrial fragmentation in HT-22 hippocampal neuron cells that were incubated with ferric ammonium citrate (FAC). Mitochondrial fragmentation via dephosphorylation of Drp1 (Ser637) and increased apoptotic neuronal death were observed in FAC-stimulated HT-22 cells. Furthermore, the levels of intracellular calcium (Ca 2+ ) were increased by iron overload. Notably, chelation of intracellular Ca 2+ rescued mitochondrial fragmentation and neuronal cell death. In addition, iron overload activated calcineurin through the Ca 2+ /calmodulin and Ca 2+ /calpain pathways. Pretreatment with the calmodulin inhibitor W13 and the calpain inhibitor ALLN attenuated iron overload-induced mitochondrial fragmentation and neuronal cell death. Therefore, these findings suggest that Ca 2+ -mediated calcineurin signals are a key player in iron-induced neurotoxicity by regulating mitochondrial dynamics. We believe that our results may contribute to the development of novel therapies for iron toxicity related neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

Mutations in Frataxin (FXN) cause Friedreich's ataxia (FRDA), a recessive neurodegenerative disorder. Previous studies have proposed that loss of FXN causes mitochondrial dysfunction, which triggers elevated reactive oxygen species (ROS) and leads to the demise of neurons. Here we describe a ROS independent mechanism that contributes to neurodegeneration in fly FXN mutants. We show that loss of frataxin homolog (fh) in Drosophila leads to iron toxicity, which in turn induces sphingolipid synthesis and ectopically activates 3-phosphoinositide dependent protein kinase-1 (Pdk1) and myocyte enhancer factor-2 (Mef2). Dampening iron toxicity, inhibiting sphingolipid synthesis by Myriocin, or reducing Pdk1 or Mef2 levels, all effectively suppress neurodegeneration in fh mutants. Moreover, increasing dihydrosphingosine activates Mef2 activity through PDK1 in mammalian neuronal cell line suggesting that the mechanisms are evolutionarily conserved. Our results indicate that an iron/sphingolipid/Pdk1/Mef2 pathway may play a role in FRDA. [ABSTRACT FROM AUTHOR]

Background Many chronic diseases are adversely affected by elevated iron levels. It has been speculated that this relationship is mediated by increased oxidative stress, due to the ability of iron to generate reactive oxygen species. The aim of this study was to assess the relationship between elevated iron levels and lipid peroxidation in Caucasian adults residing in the north-eastern Mediterranean region of Spain. Materials and methods This cross-sectional case-control study included 300 subjects: 150 adults displaying elevated iron levels (cases) selected from a representative sample of our general population and 150 age- and sex-matched adults exhibiting normal iron levels (controls). Dietary assessment (3-day food records), iron biomarkers (serum iron, ferritin and transferrin saturation) and lipid profile were determined. Elevated iron levels were defined by high serum ferritin ( SF>110 μg/L in women and>200 μg/L in men) and/or transferrin saturation ( TS)>45%. Oxidized low-density lipoprotein (ox LDL) plasma levels were measured, and ox LDL/ LDL-cholesterol ratio was calculated to estimate lipid peroxidation. Multiple linear regression ( MLR) models were applied. Results Individuals with elevated serum iron levels showed increased ox LDL/ LDL ratio, but not ox LDL levels, compared to control subjects (20·92 ± 4·89 U/mmol vs. 19·72 ± 3·573 U/mmol, P = 0·028). These results were further confirmed by the regression models adjusted for demographic characteristics, diet, lipid profile and inflammation. Importantly, higher serum levels of triglycerides, LDL-cholesterol and lower intake of Vitamin E increased lipid peroxidation. Conclusions In our general population, we have observed that higher circulating levels of iron, measured by serum ferritin and/or TS, increased lipid peroxidation (measured by ox LDL/ LDL ratio). [ABSTRACT FROM AUTHOR]

Currently, there are increasing efforts to utilize nanoremediation as an environmental technology for cleaning up polluted environments using nanoscale zero-valent iron (nZVI); however, concerns exist regarding the long-term environmental impact of this strategy. In this study, an innovative methodology for evaluating nZVI impact on soil bacteria is utilized, based on transcriptional analysis of three novel biomakers: tnaA, sodB and trx genes. At the same time, classical toxicological bioassays with the nematode Caenorhabditis elegans were performed. Microcosms treated with 1, 5 and 10 % w/ w of nZVI were set up using a commercial standard soil and incubated for 21 days. The tnaA gene, involved in indole production, was significantly upregulated at all assessed nZVI concentrations, suggesting that bacterial cells used this molecule to inform the rest of the community about the changes produced upon nZVI soil treatment. The higher the exposure time, the lower nZVI concentration needed to detect these changes. Consequently, soil bacteria activate a cellular adaptive response to cope with the nZVI-induced oxidative stress, increasing the expression of genes encoding key reactive oxygen species (ROS)-scavenging enzymes; in fact, an upregulation of the sodB and katB genes was recorded upon nZVI exposure. On the contrary, C. elegans survival and growth endpoints were not affected at any nZVI concentration whereas the exposure time significantly increased nematode growth in the soil. Therefore, despite the lack of toxicity revealed by the classical conducted tests, the transcriptional analyses demonstrated the usefulness of combining the set of proposed biomarkers for early detection and monitoring the impact of nZVI on soil bacteria after environmentally important periods of exposure. [ABSTRACT FROM AUTHOR]

Rusty roots markedly influence on ginseng cultivation, and this phenomenon often attributed to iron (Fe) induced toxicity. To examine the physiological mechanisms underlying Fe-initiated toxicity as evidenced by rusty roots inPanax ginseng, morphological and physiological changes in roots were investigated in hydroponics using Fe2+concentrations of 50 (control), 100, 200, 400 or 600 µM. Compared with control, reddish-brown deposition at the root surface increasingly appeared as Fe2+concentration increased (≥200 µM). The pH also rose as Fe levels were elevated. Higher external Fe2+concentrations produced changes in root organelles and cell structures. Structural alterations in mitochondria due to excess Fe storage, protoplast shrinkage and cell vacuolation as well as formation of central vacuole with deposits in roots were observed. In addition, apparent cell wall thickening, cell wall folding and shrinkage, damage of cell membranes and a large amount of cell debris occurred at higher external Fe2+concentrations (≥400 µM). The Fe2+mediated damage resulting in morphological and physiological changes in ginseng roots was concentration and pH dependent. [ABSTRACT FROM PUBLISHER]

Background Iron is an essential but potentially toxic metal in mammals. Here we investigated a pathogenic role of exogenous iron in peripheral diabetic neuropathy (PDN) in an animal model for type 1 diabetes. Methods Diabetes was induced by a single injection of streptozotocin (STZ) in 4-month-old Sprague–Dawley rats. STZ-diabetic rats and non-diabetic rats were fed with high, standard, or low iron diet. After three months of feeding, animals were tested. Results STZ-rats on standard iron diet showed overt diabetes, slowed motor nerve conduction, marked degeneration of distal intraepidermal nerve fibers, mild intraneural infiltration with macrophages and T-cells in the sciatic nerve, and increased iron levels in serum and dorsal root ganglion (DRG) neurons. While motor fibers were afflicted in all STZ-groups, only a low iron-diet led also to reduced sensory conduction velocities in the sciatic nerve. In addition, only STZ-rats on a low iron diet showed damaged mitochondria in numerous DRG neurons, a more profound intraepidermal nerve fiber degeneration indicating small fiber neuropathy, and even more inflammatory cells in sciatic nerves than seen in any other experimental group. Conclusions These results indicate that dietary iron-deficiency rather than iron overload, and mild inflammation may both promote neuropathy in STZ-induced experimental PDN. [ABSTRACT FROM AUTHOR]

Iron overload is a potentially life-threatening consequence of multiple red-blood-cell transfusions. Here, we review factors affecting excess iron distribution and its damage to specific tissues, as well as mechanisms of oncogenesis by iron. Although consequences of transfusional iron overload are best described in thalassemia major and related inherited anemias, they are increasingly recognized in acquired conditions, such as myelodysplastic syndromes (MDS). Iron overload in MDS not only impacts on certain tissues, but may affect the clonal evolution of MDS through generation of reactive oxygen species. Iron overload may also influence hematopoietic-stem-cell-transplantation outcomes. Novel MRI methods for assessing body iron have impacted significantly on outcome in inherited anemias by allowing monitoring of iron burden and iron chelation therapy. This approach is increasingly being used in MDS and stem-cell-transplant procedures. Knowledge gained from managing transfusional iron overload in inherited anemias may be translated to general oncology, with potential for improved patient outcomes. [ABSTRACT FROM AUTHOR]

Summary Body iron has a very close relationship with the liver. Physiologically, the liver synthesizes transferrin, in charge of blood iron transport; ceruloplasmin, acting through its ferroxidase activity; and hepcidin, the master regulator of systemic iron. It also stores iron inside ferritin and serves as an iron reservoir, both protecting the cell from free iron toxicity and ensuring iron delivery to the body whenever needed. The liver is first in line for receiving iron from the gut and the spleen, and is, therefore, highly exposed to iron overload when plasma iron is in excess, especially through its high affinity for plasma non-transferrin bound iron. The liver is strongly involved when iron excess is related either to hepcidin deficiency, as in HFE, hemojuvelin, hepcidin, and transferrin receptor 2 related haemochromatosis, or to hepcidin resistance, as in type B ferroportin disease. It is less involved in the usual (type A) form of ferroportin disease which targets primarily the macrophagic system. Hereditary aceruloplasminemia raises important pathophysiological issues in light of its peculiar organ iron distribution. [ABSTRACT FROM AUTHOR]