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Iron Levels (iron + level)
Kinds of Iron Levels Selected AbstractsImpaired intestinal iron absorption in Crohn's disease correlates with disease activity and markers of inflammationINFLAMMATORY BOWEL DISEASES, Issue 12 2006Gaith Semrin MD Abstract Background: Anemia in patients with Crohn's disease (CD) is a common problem of multifactorial origin, including blood loss, malabsorption of iron, and anemia of inflammation. Anemia of inflammation is caused by the effects of inflammatory cytokines [predominantly interleukin-6 (IL-6)] on iron transport in enterocytes and macrophages. We sought to elucidate alterations in iron absorption in pediatric patients with active and inactive CD. Methods: Nineteen subjects with CD (8 female, 11 male patients) were recruited between April 2003 and June 2004. After an overnight fast, serum iron and hemoglobin levels, serum markers of inflammation [IL-6, C-reactive protein (CRP), and erythrocyte sedimentation rate], and a urine sample for hepcidin assay were obtained at 8 am. Ferrous sulfate (1 mg/kg) was administered orally, followed by determination of serum iron concentrations hourly for 4 hours after the ingestion of iron. An area under the curve for iron absorption was calculated for each patient data set. Results: There was a strong inverse correlation between the area under the curve and IL-6 (P = 0.002) and area under the curve and CRP levels (P = 0.04). Similarly, the difference between baseline and 2-hour serum iron level (,[Fe]2hr) correlated with IL-6 (P = 0.008) and CRP (P = 0.045). When cutoff values for IL-6 (>5 pg/mL) and CRP (>1.0 mg/dL) were used, urine hepcidin levels also positively correlated with IL-6 and CRP levels (P = 0.003 and 0.007, respectively). Conclusions: Subjects with active CD have impaired oral iron absorption and elevated IL-6 levels compared with subjects with inactive disease. These findings suggest that oral iron may be of limited benefit to these patients. Future study is needed to define the molecular basis for impaired iron absorption. [source] ORIGINAL ARTICLE: Effect of Lactobacillus fermentum and Enterococcus faecium strains on internal milieu, antioxidant status and body weight of broiler chickensJOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 5 2010M. Capcarova Summary The aim of the present study was to evaluate the functional efficiency of two probiotic strains Lactobacillus fermentum CCM 7158 and Enterococcus faecium M 74 given to the drinking water on internal milieu, antioxidant status and body weight of broiler chickens. The experiment was conducted on hybrid Hybro (n = 180). The feeding period lasted 42 days. Experimental chickens of E1 group received a probiotic preparation in drinking water with concentration of 1 × 109 colony forming units (CFU) of L. fermentum CCM 7158 in 1 g of nutrient medium and experimental chickens of E2 group concentration of 2 × 109 CFU of E. faecium M 74 in 1 g of nutrient medium. The control group of animals received water without any additives. Triglycerides content in serum mainly with L. fermentum strain against the control group was decreased. Calcium content in both experimental groups and significantly in E. faecium group was increased. Antioxidant status in both probiotic groups was significantly increased. The content of bilirubin in group with E. faecium M 74 was significantly increased. In conclusion, addition of a microbial feed additive (L. fermentum and E. faecium) increased serum calcium and iron level, decreased triglycerides content in blood and slightly increased body weight of broiler chickens. [source] Haemopexin affects iron distribution and ferritin expression in mouse brainJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 10 2009Noemi Morello Abstract Haemopexin (Hx) is an acute phase plasma glycoprotein, mainly produced by the liver and released into plasma where it binds heme with high affinity and delivers it to the liver. This system provides protection against free heme-mediated oxidative stress, limits access by pathogens to heme and contributes to iron homeostasis by recycling heme iron. Hx protein has been found in the sciatic nerve, skeletal muscle, retina, brain and cerebrospinal fluid (CSF). Recently, a comparative proteomic analysis has shown an increase of Hx in CSF from patients with Alzheimer's disease, thus suggesting its involvement in heme detoxification in brain. Here, we report that Hx is synthesised in brain by the ventricular ependymal cells. To verify whether Hx is involved in heme scavenging in brain, and consequently, in the control of iron level, iron deposits and ferritin expression were analysed in cerebral regions known for iron accumulation. We show a twofold increase in the number of iron-loaded oligodendrocytes in the basal ganglia and thalamus of Hx-null mice compared to wild-type controls. Interestingly, there was no increase in H- and L-ferritin expression in these regions. This condition is common to several human neurological disorders such as Alzheimer's disease and Parkinson's disease in which iron loading is not associated with an adequate increase in ferritin expression. However, a strong reduction in the number of ferritin-positive cells was observed in the cerebral cortex of Hx-null animals. Consistent with increased iron deposits and inadequate ferritin expression, malondialdehyde level and Cu,Zn superoxide dismutase-1 expression were higher in the brain of Hx-null mice than in that of wild-type controls. These data demonstrate that Hx plays an important role in controlling iron distribution within brain, thus suggesting its involvement in iron-related neurodegenerative diseases. [source] Oxidative-inflammatory damage in cirrhosis: Effect of vitamin E and a fermented papaya preparationJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2007Francesco Marotta Abstract Background and Aim:, Oxidative DNA damage occurs as an early event in hepatitis C virus (HCV) infection and is an indication of the potential for carcinogenesis. The aim of this study was to test a novel antioxidant/immunomodulator in patients with HCV-related cirrhosis. Methods:, The study group consisted of 50 patients with HCV-related cirrhosis with transaminase values less than twofold increased (alanine aminotransferase [ALT] < 80 IU/L). Patients underwent a standardized food-vitamin composition assessment and were assessed for dietary intake, nutritional status and iron level. Patients were randomly allocated into two groups and then given either ,-tocopherol 900 IU/day or 9 g/day of a fermented papaya preparation (FPP, Immun-Age, Osato Research Institute, Gifu, Japan) at bedtime for 6 months. Ten healthy subjects served as controls. Patients were checked monthly for: routine tests, redox status (reduced glutathione, glutathione peroxidase, oxidized glutathione, malondialdehyde), plasma ,-tocopherol, 8-hydroxy-deoxy-guanidine (8-OHdG) level in circulating leukocyte DNA and serum levels of cytokines. Results:, Patients with cirrhosis showed a significant imbalance of redox status (low antioxidants/high oxidative stress markers) (P < 0.005 vs controls). Neither treatment regimen affected transaminases as a whole. However, vitamin E supplementation almost normalized ALT only in the limited vitamin-E-deficient subgroup. A significant improvement of redox status was obtained by both regimens. However, only FPP significantly decreased 8-OHdG and the improvement of cytokine balance with FPP was significantly better than with vitamin E treatment (P < 0.05). Conclusions:, Although the present data seem to suggest a potential supportive role of antioxidants/immunomodulators as FPP in HCV patients, more studies are needed to substantiate their effect on the natural history of the disease. [source] Growth, haematological parameters and tissue lipid peroxidation of soft-shelled turtles, Pelodiscus sinensis, fed diets supplemented with different levels of ferrous sulphateAQUACULTURE NUTRITION, Issue 1 2009J.-H. CHU Abstract Soft-shelled turtles, Pelodiscus sinensis, with an average weight of 5.55 g, were fed diets supplemented with eight levels of ferrous sulphate for 8 weeks. The analysed iron content ranged from 50.8 to 482.9 mg kg,1. Growth rate of turtles fed the control diet with no iron supplementation was the lowest among all dietary groups. Haematological parameters including red blood cell, haemoglobin, haematocrit, mean corpuscular volume, mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration of the turtles fed the control diet were also significantly (P < 0.05) lower relative to the other groups. Thus, dietary iron at 50.8 mg kg,1 (no supplemented iron) was deemed deficient for growth and ineffective at preventing anaemia in juvenile soft-shelled turtle. Whereas, a supplementation of 50 mg kg,1 ferrous sulphate (a total dietary iron of 91.8 mg kg,1) was enough to normalize the haematological values of soft-shelled turtles to the level similar to other iron supplement-fed groups. Within the tested dietary iron range, liver iron content curve-linearly (r2 = 0.99) increased with increasing dietary iron level. Furthermore, thiobarbituric acid-reactive substances in liver tissues of the turtles have also increased when liver iron content increased. The dietary iron requirement of soft-shelled turtle is 120,198 mg kg,1 when ferrous sulphate is used as the source of iron. [source] Iron enhances endothelial cell activation in response to Cytomegalovirus or Chlamydia pneumoniae infectionEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2006A. E. R. Kartikasari Abstract Background, Chronic inflammation has been implemented in the pathogenesis of inflammatory diseases like atherosclerosis. Several pathogens like Chlamydia pneumoniae (Cp) and cytomegalovirus (CMV) result in inflammation and thereby are potentially artherogenic. Those infections could trigger endothelial activation, the starting point of the atherogenic inflammatory cascade. Considering the role of iron in a wide range of infection processes, the presence of iron may complicate infection-mediated endothelial activation. Materials and methods, Endothelial intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelial selectin (E-selectin) expression were measured using flow cytometry, as an indication of endothelial activation. Cytotoxicity was monitored using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Immunostaining was applied to measure Cp and CMV infectivity to endothelial cells. Results, An increased number of infected endothelial cells in a monolayer population leads to a raised expression of adhesion molecules of the whole cell population, suggesting paracrine interactions. Iron additively up-regulated Cp-induced VCAM-1 expression, whereas synergistically potentiated Cp-induced ICAM-1 expression. Together with CMV, iron also enhanced ICAM-1 and VCAM-1 expression. These iron effects were observed without modulation of the initial infectivity of both microorganisms. Moreover, the effects of iron could be reversed by intracellular iron chelation or radical scavenging, conforming modulating effects of iron on endothelial activation after infections. Conclusions, Endothelial response towards chronic infections depends on intracellular iron levels. Iron status in populations positive for Cp or CMV infections should be considered as a potential determinant for the development of atherosclerosis. [source] MIXTURES OF BEEF TRIPE, BEEF LIVER AND SOYBEANS APPLIED TO FOOD DEVELOPMENTJOURNAL OF FOOD PROCESSING AND PRESERVATION, Issue 3 2007L. MALVESTITI ABSTRACT A nutritive sausage-type product was developed with beef tripe, beef liver and soybeans as ingredients. A three-component mixture design was used to obtain seven different formulations (minimum of each main ingredient: 16.5%, maximum: 67.0%). Ingredients were ground, mixed and packed tightly with a polypropylene film to obtain a roll. Pieces were cooked in boiling water for 90 min. The composition of the obtained products varied within the following ranges: proteins 17.32,25.56 g/100 g, lipids 3.22,3.87 g/100 g, crude fiber 1.50,4.50 g/100 g, minerals 1.44,2.72 g/100 g. Total iron levels varied between 1.39 and 2.98 mg/100 g and calcium levels between 15.07 and 34.01 mg/100 g. Surface response analysis was applied to parameters obtained from texture profile analysis (hardness, adhesiveness, cohesiveness and elasticity). Products hardness increased when the soy content increased; on the contrary, formulations enriched in beef tripe were those of higher elasticity and cohesiveness. Color was mainly determined by the incorporation of liver. A nontrained panel was used to evaluate the acceptance of the different formulations. The most accepted one was that with equal proportions of the three main ingredients. Microbiological challenge testing showed that the thermal treatment was enough for assuring the product safeness even in samples with high initial microbial charge. [source] Temporal responses in the disruption of iron regulation by manganeseJOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2006Catherine Kwik-Uribe Abstract Manganese (Mn) is an essential trace element, though at elevated exposures it is also a neurotoxicant. Several mechanisms underlying manganese toxicity have been investigated, although a consistent mechanism(s) of action at low exposures has not been fully elucidated. Here we systematically evaluated the effects of in vitro manganese exposure on intracellular iron (Fe) homeostasis and iron-regulatory protein (IRP) binding activity in undifferentiated PC12 cells over a range of manganese exposure concentrations (1, 10, 50, and 200 ,M MnCl2) and exposure durations (12, 24, 36, and 48 hr), to test the hypothesis that moderately elevated manganese exposure disrupts cellular iron regulation. Results demonstrate that manganese exposure produces a rapid and sustained dose-dependent dysregulation of cellular iron metabolism, with effects occurring as early as 12 hr exposure and at manganese doses as low as 1 ,M. Manganese exposure altered the dynamics of IRP-1 binding and the intracellular abundance of IRP-2, and altered the cellular abundance of transferrin receptor, ferritin, and mitochondrial aconitase protein levels. Cellular levels of labile iron were significantly increased with manganese exposure, although total cellular iron levels were not. The overall pattern of effects shows that manganese produced an inappropriate cellular response akin to iron deficiency, to which the cells were able to mount a compensatory response. Consistent with our previous studies, these data indicate that even low to moderate exposures to Manganese in vitro significantly disrupt cellular iron metabolism, which may be an important contributory mechanism of manganese neurotoxicity. © 2006 Wiley-Liss, Inc. [source] Design, synthesis and properties of novel iron(III)-specific fluorescent probesJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 4 2004Wei Luo ABSTRACT Bidentate chelators such as hydroxypyridinones and hydroxypyranones are highly iron selective. The synthesis of two novel fluorescent probes N -[2-(3-hydroxy-2-methyl-4-oxopyridin-1(4H)-yl)ethyl]-2-(7-methoxy-2-oxo-2H -chromen-4-yl)acetamide (CP600) and N -[(3-hydroxy-6-methyl-4-oxo-4H -pyran-2-yl)methyl]-2-(7-methoxy-2-oxo-2H -chromen-4-yl)acetamide (CP610) is reported. The method involves coupling the bidentate ligands, 3-hydroxypyridin-4-one and 3-hydroxypyran-4-one, with the well-characterised fluorescent probe methoxycoumarin. Fluorescence emission of both probes at 380 nm is readily quenched by Fe3+. The fluorescence was quenched to a greater extent by Fe3+ than by Mn2+, Co2+, Zn2+, Ca2+, Mg2+, Na+ and K+ and to approximately the same extent as Cu2+. Comparison of the fluorescence-quenching ability by a range of metal ions on CP600 and CP610 and the hexadentate chelator, calcein, under in-vitro conditions, demonstrated advantages of the two novel fluorescent probes with respect to both iron(III) sensitivity and selectivity. Chelation of iron(III) by CP600 and CP610 leads to the formation of a complex with a metal-to-ligand ratio of 1:3. Fluorescence is quenched on formation of such complexes. These probes possess a molecular weight less than 400 and thus they are predicted to permeate biological membranes by passive diffusion, and have potential for reporting intracellular organelle labile iron levels. [source] Effects of Alcohol Consumption on Iron Metabolism in Mice with Hemochromatosis MutationsALCOHOLISM, Issue 1 2007Jonathan M. Flanagan Background: Alcoholic liver disease is associated with increased hepatic iron accumulation. The liver-derived peptide hepcidin is the central regulator of iron homeostasis and recent animal studies have demonstrated that exposure to alcohol reduces hepcidin expression. This down-regulation of hepcidin in vivo implies that disturbed iron sensing may contribute to the hepatosiderosis seen in alcoholic liver disease. Alcohol intake is also a major factor in expression of the hemochromatosis phenotype in patients homozygous for the C282Y mutation of the HFE gene. Methods: To assess the effect of alcohol in mice with iron overload, alcohol was administered to mice with disrupted Hfe and IL-6 genes and Tfr2 mutant mice and their respective 129x1/SvJ, C57BL/6J, and AKR/J wild-type congenic strains. Iron absorption, serum iron levels, and hepcidin expression levels were then measured in these mice compared with water-treated control mice. Results: Alcohol was shown to have a strain-specific effect in 129x1/SvJ mice, with treated 129x1/SvJ mice showing a significant increase in iron absorption, serum iron levels, and a corresponding decrease in hepcidin expression. C57BL/6J and AKR/J strain mice showed no effect from alcohol treatment. 129x1/SvJ mice heterozygous or homozygous for the Hfe knockout had a diminished response to alcohol. All 3 strains were shown to have high blood alcohol levels. Conclusions: The effect of alcohol on iron homeostasis is dependent on the genetic background in mice. In an alcohol-susceptible strain, mutation of the Hfe gene diminished the response of the measured iron indices to alcohol treatment. This indicates that either maximal suppression of hepcidin levels had already occurred as a result of the Hfe mutation or that Hfe was a component of the pathway utilized by EtOH in suppressing hepcidin production and increasing iron absorption. [source] A Review of Genetic, Biological, Pharmacological, and Clinical Factors That Affect Carbohydrate-Deficient Transferrin LevelsALCOHOLISM, Issue 9 2004Michael F. Fleming Background: Carbohydrate-deficient transferrin (CDT) is an alcohol biomarker recently approved by the U.S. Food and Drug Administration. This test is increasingly being used to detect and monitor alcohol use in a variety of health care, legal, and industrial settings. The goal of this study is to review the genetic, biological, pharmacological, and clinical factors that may affect CDT levels. Methods: A review of the literature identified 95 research articles that met the authors' criteria and reported potential interactions of a variety of factors on percent and total CDT levels. The review established 12 categories of variables that may affect CDT levels. These categories include (1) alcohol use, (2) genetic factors, (3) race, (4) gender, (5) age, (6) liver disease, (7) iron levels, (8) tobacco use, (9) medication such as estrogen and anticonvulsants, (10) metabolic factors such as body mass index and total body water, (11) chronic medical conditions such as rheumatoid arthritis, and (12) surgical patients. Results: There is evidence that %CDT levels are affected by alcohol use, end-stage liver disease, and genetic variants. In addition to these three factors, total CDT levels (CDTect) are also affected by factors that raise transferrin levels such as iron deficiency, chronic illnesses, and menopausal status. Other potential factors such as tobacco and age appear to be confounded by alcohol use. The roles of female gender, low body mass index, chronic inflammatory diseases, and medication on CDT levels require further study. False negatives are associated with female gender, episodic lower level alcohol use, and acute trauma with blood loss. Conclusions: This review suggests that a number of factors are associated with false-positive CDTect and %CDT levels. CDT offers great promise to assist physicians in the care of patients to detect and monitor heavy alcohol use. [source] Influence of HFE gene polymorphism on the progression and treatment of chronic hepatitis CJOURNAL OF VIRAL HEPATITIS, Issue 2 2004P. Lebray Summary., We analysed liver histology findings in a large cohort of patients with chronic hepatitis C and in roughly half of them their response to interferon- , -based on iron parameters and HFE status. Histological activity and virological response to antiviral therapy (n = 146) were analysed in 273 immunocompetent and nonalcoholic patients with chronic hepatitis C, in terms of serum iron load, intrahepatic iron load (n = 110) and HFE mutations. Patients who were heterozygous for the C282Y and H63D mutations exhibited higher iron serum parameters than subjects without these mutations. The intrahepatic iron load was higher in H63D patients only. No association was observed between HFE mutations and histological activity. Increased iron parameters were associated with liver disease severity by univariate analysis only. Genotype 1 and ferritinaemia were associated with a poor response to antiviral therapy, whereas the H63D mutation emerged as a positive predictive factor for end of treatment and sustained antiviral response. Therefore, in chronic hepatitis C patients serum and intrahepatic iron levels were weakly correlated with histological activity, while HFE mutations were not. As for the response to interferon- ,, elevated ferritinaemia constituted a negative predictive factor whereas the H63D mutation was a positive one. The H63D mutation might form part of an immunogenetic profile influencing the response to interferon therapy. [source] Liver transplantation for hereditary hemochromatosisLIVER TRANSPLANTATION, Issue 8 2001David J. Brandhagen MD Although hereditary hemochromatosis (HHC) is relatively common, it is an uncommon indication for orthotopic liver transplantation (OLT). The diagnosis of HHC in patients with end-stage liver disease is difficult because many of these patients have elevated serum and tissue iron levels. Of patients undergoing OLT with iron stores in the range typical for HHC, approximately 10% are homozygous for the C282Y mutation. Most studies published to date noted decreased survival in patients who underwent OLT for HHC compared with those who underwent OLT for other indications. Death in patients with HHC was caused by increased infectious and cardiac complications. Decreased post-OLT survival in patients with iron overload appears to be independent of HFE gene status. This suggests that regardless of the cause, iron overload may be detrimental in patients undergoing OLT. Follow-up of patients undergoing OLT for HHC and case reports of the inadvertent transplantation of a liver from a donor with HHC has furthered our understanding of the pathophysiological state of iron overload in HHC. [source] Damped oscillations in the adaptive response of the iron homeostasis network of E. coliMOLECULAR MICROBIOLOGY, Issue 2 2010Amnon Amir Summary Living organisms often have to adapt to sudden environmental changes and reach homeostasis. To achieve adaptation, cells deploy motifs such as feedback in their genetic networks, endowing the cellular response with desirable properties. We studied the iron homeostasis network of E. coli, which employs feedback loops to regulate iron usage and uptake, while maintaining intracellular iron at non-toxic levels. Using fluorescence reporters for iron-dependent promoters in bulk and microfluidics-based, single-cell experiments, we show that E. coli cells exhibit damped oscillations in gene expression, following sudden reductions in external iron levels. The oscillations, lasting for several generations, are independent of position along the cell cycle. Experiments with mutants in network components demonstrate the involvement of iron uptake in the oscillations. Our findings suggest that the response is driven by intracellular iron oscillations large enough to induce nearly full network activation/deactivation. We propose a mathematical model based on a negative feedback loop closed by rapid iron uptake, and including iron usage and storage, which captures the main features of the observed behaviour. Taken together, our results shed light on the control of iron metabolism in bacteria and suggest that the oscillations represent a compromise between the requirements of stability and speed of response. [source] Submicromolar hydrogen peroxide disrupts the ability of Fur protein to control free-iron levels in Escherichia coliMOLECULAR MICROBIOLOGY, Issue 3 2007Shery Varghese Summary In aerobic environments, mutants of Escherichia coli that lack peroxidase and catalase activities (Hpx,) accumulate submicromolar concentrations of intracellular H2O2. We observed that in defined medium these strains constitutively expressed members of the Fur regulon. Iron-import proteins, which Fur normally represses, were fully induced. H2O2 may antagonize Fur function by oxidizing the Fur:Fe2+ complex and inactivating its repressor function. This is a potential problem, as in iron-rich environments excessive iron uptake would endanger H2O2 -stressed cells by accelerating hydroxyl-radical production through the Fenton reaction. However, the OxyR H2O2 -response system restored Fur repression in iron-replete Luria,Bertani medium by upregulating the synthesis of Fur protein. Indeed, when the OxyR binding site upstream of fur was disrupted, Hpx, mutants failed to repress transporter synthesis, and they exhibited high levels of intracellular free iron. Mutagenesis and bacteriostasis resulted. These defects were eliminated by mutations or chelators that slowed iron import, confirming that dysregulation of iron uptake was the root problem. Thus, aerobic organisms must grapple with a conundrum: how to monitor iron levels in oxidizing environments that might perturb the valence of the analyte. The induction of Fur synthesis by the OxyR response comprises one evolutionary solution to that problem. [source] Serological levels of zinc, copper and iron elements among Giardia lamblia infected children in TurkeyPEDIATRICS INTERNATIONAL, Issue 3 2002Pelin Ertan Abstract Background: Giardiasis, an intestinal protozoan infection caused by Giardia lamblia, is common in Turkey, especially among children aged between 2- and 14-years-old. Effects of giardiasis on serological levels of zinc, copper and iron elements were assessed in this study. Methods: A total of 45 children, aged between 2- and 14-years-old, who were admitted to the Pediatrics Department of Celal Bayar University Medical School with gastrointestinal complaints and diagnosed as having giardiasis by stool examinations in the Parasitology Department, were enrolled as the study group (SG). The control group (CG) consisted of 45 age-matched healthy children. Serological levels of zinc, copper and iron were measured by atomic absorption spectrophotometer in all samples. Results: As a result of the study, serum zinc levels were 67.43 ± 17.72 µg/dL and 145.20 ± 9.13 µg/dL, copper levels were 198.45 ± 39.14 µg/dL and 150 ± 21.14 µg/dL and iron levels were 87.98 ± 18.31 µg/dL and 160.45 ± 45.40 µg/dL, in SG and CG, respectively. When compared separately as SG and CG, there was a statistically significant difference between the serological levels of all these elements. Conclusion: These results revealed that giardiasis increased the serological levels of copper, like other infectious agents. However, zinc and iron levels decreased during giardiasis due to malabsorption. [source] Mechanisms of iron loading and toxicityAMERICAN JOURNAL OF HEMATOLOGY, Issue S12 2007Gregory J. Anderson Normal iron homeostasis is a finely balanced system that reflects iron absorption, loss and utilization. The body has no mechanism for the active excretion of iron, so body iron levels are controlled at the point of absorption in the small intestine. Disturbances in this equilibrium, such as those leading to enhanced absorption, can have significant clinical consequences. Continued excessive iron uptake is followed by iron deposition in various tissues, ultimately leading to tissue damage, and possibly end-organ failure. In this review, current concepts in normal iron homeostasis, and iron loading are explained. The clinical consequences as well as the differences between primary and secondary iron loading are also reviewed, and some future research priorities are discussed. Am. J. Hematol., 2007. © 2007 Wiley-Liss, Inc. [source] Acute toxicity in five dogs after ingestion of a commercial snail and slug bait containing iron EDTAAUSTRALIAN VETERINARY JOURNAL, Issue 7 2009SL Haldane This case series of five dogs describes the effects of ingesting large amounts of an iron EDTA snail-bait product. In all cases signs of toxicity occurred between 6 and 24 h after ingestion and included abdominal pain and haemorrhagic gastroenteritis. Two of the dogs had pretreatment serum iron levels measured and in both cases the levels were above normal limits. All of the dogs were treated with iron chelation therapy and supportive care including intravenous fluids, analgesics, gastric protectants and antibiotics. Chelation therapy with desferrioxamine mesylate did not cause adverse effects in any of the dogs and all survived to discharge. The effects of iron EDTA snail bait in dogs requires further study and minimum toxic doses need to be established. [source] Regulatory mechanisms of intestinal iron absorption,Uncovering of a fast-response mechanism based on DMT1 and ferroportin endocytosisBIOFACTORS, Issue 2 2010Marco T. Núñez Abstract Knowledge on the intestinal iron transport process and the regulation of body iron stores has greatly increased during the last decade. The liver, through the sensing of circulating iron, is now recognized as the central organ in this regulation. High iron levels induce the synthesis of hepcidin, which in turn decreases circulating iron by inhibiting its recycling from macrophages and its absorption at the intestine. Another mechanism for the control of iron absorption by the enterocyte is an active Iron Responsive Element (IRE)/Iron Regulatory Protein (IRP) system. The IRE/IRP system regulates the expression of iron uptake and storage proteins thus regulating iron absorption. Similarly, increasing evidence points to the transcriptional regulation of both divalent metal transporter 1 (DMT1) and ferroportin expression. A new mechanism of regulation related to a phenomenon called the mucosal block is starting to be unveiled. The mucosal block describes the ability of an initial dose of ingested iron to block absorption of a second dose given 2,4 h later. Here, we review the mechanisms involved in the expression of DMT1 and ferroportin, and present recent evidence on the molecular components and cellular processes involved in the mucosal block response. Our studies indicate that mucosal block is a fast-response endocytic mechanism destined to decrease intestinal iron absorption during a high ingest of iron. [source] Impact of daily consumption of iron fortified ready-to-eat cereal and pumpkin seed kernels (Cucurbita pepo) on serum iron in adult womenBIOFACTORS, Issue 1 2007Mohammad Reza Naghii Abstract Iron deficiency, anemia, is the most prevalent nutritional problem in the world today. The objective of this study was to consider the effectiveness of consumption of iron fortified ready-to-eat cereal and pumpkin seed kernels as two sources of dietary iron on status of iron nutrition and response of hematological characteristics of women at reproductive ages. Eight healthy female, single or non pregnant subjects, aged 20,37 y consumed 30 g of iron fortified ready-to-eat cereal (providing 7.1 mg iron/day) plus 30 g of pumpkin seed kernels (providing 4.0 mg iron/day) for four weeks. Blood samples collected on the day 20 of menstrual cycles before and after consumption and indices of iron status such as reticulocyte count, hemoglobin (Hb), hematocrit (Ht), serum ferritin, iron, total iron-binding capacity (TIBC), transferrin and transferrin saturation percent were determined. Better response for iron status was observed after consumption period. The statistical analysis showed a significant difference between the pre and post consumption phase for higher serum iron (60 ± 22 vs. 85 ± 23 ug/dl), higher transferrin saturation percent (16.8 ± 8.0 vs. 25.6 ± 9.0%), and lower TIBC (367 ± 31 vs. 339 ± 31 ug/dl). All individuals had higher serum iron after consumption. A significant positive correlation (r = 0.981, p = 0.000) between the differences in serum iron levels and differences in transferrin saturation percentages and a significant negative correlation (r = ,0.916, p < 0.001) between the differences in serum iron levels and differences in TIBC was found, as well. Fortified foods contribute to maintaining optimal nutritional status and minimizing the likelihood of iron insufficiencies and use of fortified ready-to-eat cereals is a common strategy. The results showed that adding another food source of iron such as pumpkin seed kernels improves the iron status. Additional and longer studies using these two food products are recommended to further determine the effect of iron fortification on iron nutrition and status among the target population, and mainly in young children, adolescents, women of reproductive ages and pregnant women. [source] Toxicological effects of iron on intestinal cellsCELL BIOCHEMISTRY AND FUNCTION, Issue 3 2004Bettina Zödl Abstract The aim of the present study was to investigate whether iron, which is involved in the formation of free radicals in vitro, can initiate cellular injury in human intestinal cells. The effects of various concentrations of iron were studied in preconfluent, colonic-cancerogenous cells, and also in postconfluent, differentiating cells. Cellular damage was assessed using cell proliferation (serial cell counting), tetrazolium dye (MTT) uptake, lactate dehydogenase (LDH) release and apoptosis studies based on caspase-3 activities. Also the activities of the major antioxidative enzymes, superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) were measured after the cells had been exposed to iron. Our results indicated that preconfluent cells were more susceptible to iron toxicity, as assessed by a significant reduction in cell proliferation and MTT uptake in a concentration-dependent manner compared to the control. However, no evidence for MTT uptake was observed in postconfluent cells. Caspase-3 activity, an indicator of cell apoptosis, considerably increased in preconfluent cells at high iron levels compared to the control (p <,0.05), whereas postconfluent cells were not significantly affected. LDH release was similar for both groups and was significantly higher than the control at 900,,M iron and above. SOD activities were not affected by iron in either group, whereas GPx was considerably higher in iron-treated cells in both groups compared with the control (because of relatively high standard deviations this effect was not significant). In conclusion we suggest that iron exerts its toxic effects intracellularly especially in preconfluent Caco-2 cells, whereas only high iron doses were able to alter the viability of differentiating, enterocyte-like cells. Copyright © 2003 John Wiley & Sons, Ltd. [source] ENDOPLASMIC RETICULUM STRESS INVOLVED IN HEART AND LIVER INJURY IN IRON-LOADED RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2009Li-Xia Lou SUMMARY 1Iron overload contributes to the pathogenesis of various diseases and directly induces tissue injury. In the present study, we investigated the relationship between heart and liver injury induced by iron overload and cellular endoplasmic reticulum (ER) stress to explore the molecular mechanism of iron overload-induced cellular injury. 2Iron overload in rats was generated by intraperitoneal injection of iron,dextran chronically (30 mg/kg per day for 9 weeks) or acutely (300 mg/kg once). Tissue injury was assessed by determining serum lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity, as well as malondialdehyde (MDA) content in the heart and liver. The ER stress response was analysed by expression of glucose-response protein 78 (GRP78) and activation of caspase 12. 3In chronic iron-loaded rats, iron levels in the heart and liver were higher, by approximately 2-and 7.8-fold, respectively (P < 0.01), compared with control. Serum LDH, ALT and AST activity, as well as MDA content, GRP78 expression and caspase 12 activity in the heart and liver, were upregulated in chronically iron-loaded rats. In acute iron-loaded rats, iron content in the heart and liver was 51% and 63% higher than in controls (both P < 0.01). Serum LDH, ALT and AST activity, MDA content in the heart and liver and levels of ER stress markers were all increased in acute iron-loaded rats. N -Acetylcysteine (150 mg/kg, s.c.) lowered the levels of these parameters in acute iron-loaded rats. 4The results of the present study indicate that ER stress may play an important role in iron-induced tissue injury and that reactive oxygen species may mediate the ER stress response in the pathogenesis of iron-overload cellular injury. [source] | ||||||||||||||||