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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the protective role of the pineal hormone melatonin on lead-induced suppression of the heme synthesis pathway as a consequence of reduced antioxidant systems in rat. We injected rats intramuscularly with lead acetate (10 mg/kg body weight) daily for 7 days, which significantly abolished heme synthesis as evidenced by decreased blood hemoglobin, liver delta-aminolevulinic acid synthetase, erythrocytic delta-aminolevulinic acid dehydratase, and hepatic iron content. These effects were accompanied with marked elevation of hepatic lipid peroxidation and decreased enzymatic antioxidants such as glutathione reductase, glutathione-S-transferase, superoxide dismutase, and catalase, as well as nonenzymatic antioxidants such as total sulfhydryl groups and glutathione. Furthermore, lead treatment caused hepatic deficiency in copper and zinc accompanied by a significant elevation of lead concentration in both plasma and liver. Daily pretreatment with melatonin (30 mg/kg body weight) intragastrically prevented the suppressive effects of lead on heme-synthesizing enzymes and iron deficiency. In addition, preadministration of melatonin reduced the inhibitory effect of lead on both enzymatic and nonenzymatic antioxidants. This was accompanied by marked normalization of lipid peroxidation and modulation of copper and zinc levels in liver. The action of melatonin on lead-induced changes was attributed to protection of the antioxidant capacity in cells in addition to the ability of melatonin to scavenge free radicals.
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PMID:Prophylactic effect of melatonin on lead-induced inhibition of heme biosynthesis and deterioration of antioxidant systems in male rats. 1056 Oct 83

Dietary copper (Cu) deficiency impairs both innate and acquired branches of immunity. Specific roles of Cu in the activation and effector activities of host-defense cells remain largely unknown. The effects of Cu status on effector activities of a monocytic cell line were investigated as an initial step in the elucidation of specific functions of Cu in phagocytic cells. Exposure of differentiating U937 human promonocytic cells to 5 micromol/L 2,3, 2-tetraamine (tet), a high affinity Cu chelator, for 4 d decreased cellular Cu by 62% without altering cellular Cu,Zn-superoxide dismutase (SOD) activity, Zn content, mitochondrial activity and protein synthesis. In contrast, Cu deficiency suppressed the respiratory burst activity and markedly compromised the ability of U937 cells to kill Salmonella. Similarly, treatment of RAW264.7 murine macrophages with 5 micromol/L tet decreased cell Cu by 78% and Cu,Zn-SOD activity by 15% and increased bacterial survival by 180%. The tet-induced impairment of respiratory burst and bactericidal activities was blocked in cultures supplemented with Cu, but not Zn or Fe. In addition, lipopolysaccharide (LPS)-induced secretion of the inflammatory mediators, tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6 and prostaglandin E(2) (PGE(2)), was decreased by 30-60% in tet-treated U937 cells. Flow cytometric analysis of the surface antigens CD11b and CD71 showed that the suppressed activities of Cu-deficient cells were not due to an attenuation in the degree of differentiation or secondary iron deficiency. These data demonstrate that U937 cells provide a useful model for examining the biochemical roles of Cu in monocyte activity.
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PMID:Copper deficiency suppresses effector activities of differentiated U937 cells. 1082 6

Iron deficiency and chronic mild carbon monoxide (CO) exposure are nutritional and environmental problems that can be experienced simultaneously. We examined the effects of chronic mild CO exposure and iron availability on auditory development in the rat. We propose that chronic mild CO exposure creates an oxidative stress condition that impairs the spiral ganglion neurons. The CO-exposed rat pups had decreased neurofilament proteins and increased copper, zinc-superoxide dismutase (SOD1) in the spiral ganglion neurons. We conclude that the increased amount of SOD1 causes an increase in hydrogen peroxide production that allows the Fenton reaction to occur. This reaction uses both iron and hydrogen peroxide to generate hydroxyl radicals and leads to the development of oxidative stress that impairs neuronal integrity. However, rat pups with decreased iron and CO exposure (ARIDCO) exhibited in their cochlea an up-regulation of transferrin, whereas their expression of neurofilament proteins and SOD1 were similar to control. Consequently, reduced iron availability and the normal expression of SOD1 do not promote oxidative stress in the cochlea. By using basal c-Fos expression as a marker for cellular activation we found a significant reduction in c-Fos expression in the central nucleus of the inferior colliculus in iron-adequate rat pups exposed to CO. By contrast, rather than being reduced, c-Fos expression in the ARIDCO group is the same as for controls. We conclude that the cochlea of rat pups with normal iron availability is selectively affected by mild CO exposure, causing a chronic oxidative stress, whereas limiting iron availability ameliorates the effect caused by mild CO exposure by averting conditions that facilitate oxidative stress.
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PMID:Limiting iron availability confers neuroprotection from chronic mild carbon monoxide exposure in the developing auditory system of the rat. 1588 Apr 90

Parenteral iron has been recommended for the treatment of iron deficiency in the majority of maintenance hemodialyzed (HD) patients. However, iron supplementation and consequent over saturation of transferrin and high iron levels, may aggravate oxidative stress already present in these patients. This study aimed to further clarify the role of repeated intravenous iron therapy as a supplementary cause of oxidative stress in HD patients. Markers of free radical activities (carbonyl reactive derivatives, CRD, thiol groups, SH, malondialdehyde, MDA) and antioxidant enzyme activities (superoxide dismutase, SOD and glutathione peroxidase, GPX) were determined in plasma and red blood cells (RBC) of 19 hemodialysis patients given a total iron dose of 625 mg (ferrogluconat, Ferrlecit, 62.5 mg). Blood samples were taken before the first and after the last dose of iron. Twenty apparently normal subjects served as healthy controls. Before iron treatment, HD patients exhibited increased concentrations of MDA and CRD in plasma and red blood cells, accompanied with impaired antioxidant capacity. All patients responded to iron therapy with a significant increase in their serum ferritin, serum iron, hemoglobin, and red blood cells levels. However, iron treatment resulted in enhanced oxidative stress in plasma of HD patients, since significant increase in plasma MDA and CRD concentrations, together with a decrease in nonprotein SH groups levels were detected. Supplementation with iron did not significantly influence plasma SOD and GPX activities, nor did any of the red blood cell parameters tested. Our data show that, despite improvement in hematological parameters, an increase in iron stores due to supplementation could also contribute to increased free radical production in HD patients.
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PMID:Evaluation of oxidative stress after repeated intravenous iron supplementation. 1595 53

Iron and copper are essential nutrients, excesses or deficiencies of which cause impaired cellular functions and eventually cell death. The metabolic fates of copper and iron are intimately related. Systemic copper deficiency generates cellular iron deficiency, which in humans results in diminished work capacity, reduced intellectual capacity, diminished growth, alterations in bone mineralization, and diminished immune response. Copper is required for the function of over 30 proteins, including superoxide dismutase, ceruloplasmin, lysyl oxidase, cytochrome c oxidase, tyrosinase and dopamine-beta-hydroxylase. Iron is similarly required in numerous essential proteins, such as the heme-containing proteins, electron transport chain and microsomal electron transport proteins, and iron-sulfur proteins and enzymes such as ribonucleotide reductase, prolyl hydroxylase phenylalanine hydroxylase, tyrosine hydroxylase and aconitase. The essentiality of iron and copper resides in their capacity to participate in one-electron exchange reactions. However, the same property that makes them essential also generates free radicals that can be seriously deleterious to cells. Thus, these seemingly paradoxical properties of iron and copper demand a concerted regulation of cellular copper and iron levels. Here we review the most salient characteristics of their homeostasis.
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PMID:Iron and copper metabolism. 1611 86

The effects of nitric oxide (NO) in protecting maize (Zea mays) leaves against iron deficiency-induced oxidative stress were investigated. The increased contents of hydrogen peroxide (H(2)O(2)) and superoxide (O(2)(-)*) due to iron deficiency suggested oxidative stress. The increased contents of thiobarbituric acid-reacting substances (TBARS) and the decreased contents of protein-bound thiol (PT) and non-protein-bound thiol (NPT) indicated iron deficiency-induced oxidative damage on proteins and lipids. Sodium nitroprusside (SNP), a nitric oxide (NO) donor, partially reversed iron deficiency-induced retardation of plant growth as well as chlorosis. Reduced contents of H(2)O(2), O(2)(-)*, TBARS and increased contents of PT and NPT also indicated that NO alleviated iron deficiency-induced oxidative damage. The activities of SOD and GR decreased sharply while the activities of CAT, POD and APX increased under SNP treatment. Our data suggest that NO can protect maize plants from iron deficiency-induced oxidative stress by reacting with ROS directly or by changing activities of ROS-scavenging enzymes.
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PMID:Protective effect of nitric oxide on iron deficiency-induced oxidative stress in maize (Zea mays). 1669 Jan 67

X-linked sideroblastic anemia with ataxia (XLSA/A) is caused by defects of the transporter ABCB7 and is characterized by mitochondrial iron deposition and excess of protoporphyrin in erythroid cells. We describe ABCB7 silencing in HeLa cells by performing sequential transfections with siRNAs. The phenotype of the ABCB7-deficient cells was characterized by a strong reduction in proliferation rate that was not rescued by iron supplementation, by evident signs of iron deficiency, and by a large approximately 6-fold increase of iron accumulation in the mitochondria that was poorly available to mitochondrial ferritin. The cells showed an increase of protoporphyrin IX, a higher sensitivity to H(2)O(2) toxicity, and a reduced activity of mitochondrial superoxide dismutase 2 (SOD2), while the activity of mitochondrial enzymes, such as citrate synthase or succinate dehydrogenase, and ATP content were not decreased. In contrast, aconitase activity, particularly that of the cytosolic, IRP1 form, was reduced. The results support the hypothesis that ABCB7 is involved in the transfer of iron from mitochondria to cytosol, and in the maturation of cytosolic Fe/S enzymes. In addition, the results indicate that anemia in XLSA/A is caused by the accumulation of iron in a form that is not readily usable for heme synthesis.
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PMID:RNA silencing of the mitochondrial ABCB7 transporter in HeLa cells causes an iron-deficient phenotype with mitochondrial iron overload. 1719 93

The present study was designed to evaluate the effect of a new iron tonic (squid ink melanin-Fe [SM-Fe]) on remission of iron deficiency anemia (IDA) using a rat model of IDA. The rat IDA model was established with low-iron diet feeding and caudal vein blooding. Then different dosages of SM-Fe were given to the rats once a day by intragastric administration, with FeSO4 and FeCl3 as positive control. The content of Hemoglobin (Hb), red blood cell (RBC), hematocrit (HCT), and mean corpuscular volume (MCV) were analyzed in addition to the contents of serum iron (SI) and intracellular free erythrocyte protoporphyrin (FEP). The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in serum was also measured. The results showed that anemia caused by iron deficiency was established as a consequence of the low-iron diets. SM-Fe showed an effective restoration action by returning Hb, RBC, HCT, MCV, SI, and FEP in IDA animals to normal values. An antioxidant effect was also observed that reduced MDA level, enhanced the activities of SOD and GSH-Px in serum, and protected erythrocytes from the injury of reactive oxygen species as a consequence of SM-Fe intake. In comparison with FeSO4 and FeCl3, higher bioavailability of iron and fewer side effects were also observed. In conclusion, SM-Fe remitted iron deficiency anemia symptoms significantly, suggesting that SM-Fe might contribute to improving hemopoietic function in IDA rats and might be exploited as a safe, efficient new iron tonic.
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PMID:Effect of squid ink melanin-Fe on iron deficiency anemia remission. 1901 17

Maintenance of iron homeostasis is of utmost importance for the respiratory system physiology and pathophysiology. Local iron deficiency or accumulation may result in particular respiratory function impairment. The aim of the present study was to find out whether iron and ferritin could be determined in exhaled breath condensate (EBC) of healthy children and children with asthma. Oxidative stress was verified by determination of EBC superoxide dismutase (SOD) activity, and the airway inflammatory process by determination of exhaled nitric oxide (F(E)NO). EBC was collected from 39 children (22 healthy children as a control group and 17 asthmatics) using an EcoScreen condenser. Iron, ferritin, and SOD were determined on optimization and validation for low concentrations. In comparison with a control group, asthma patients had a statistically significantly lower iron concentration (p = 0.0001) and higher SOD catalytic activity (p = 0.0160), with no significant difference in ferritin levels (p = 0.5252), although percentile values indicated elevated ferritin concentration in about half of asthma patients. F(E)NO values were significantly higher in the asthma group (p = 0.0047). This preliminary study demonstrated the possibility of determining iron and ferritin concentrations and SOD activity in EBC, and a significant difference in EBC iron and SOD between asthma patients and healthy children.
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PMID:Iron and ferritin concentrations in exhaled breath condensate of children with asthma. 1919 Nov 43

Physiological responses of Arabidopsis thaliana to the interaction of iron deficiency and nitrogen form were studied using plants grown in hydroponics. Thirty-three-day-old seedlings were submitted to four treatments for 7 days: NO 3 + 5 microM Fe; NO 3 + 0.1 microM Fe; NH 4 + 5 microM Fe and NH 4 + 0.1 microM Fe. Leaf growth and chlorophyll content were highest in NO 3 -fed, Fe sufficient plants, but were strongly diminished by Fe deficiency under nitric nutrition, and by ammoniacal nutrition independently of Fe regime. However, the leaves of NH 4 -fed plants presented a higher Fe content than those of Fe sufficient, NO 3 -fed plants. Thus, leaf chlorosis of NH 4 -fed in plant did not depend on Fe availability, and seemed to be due to another factor. Root acidification capacity and Fe-chelate reductase (FCR) activity were also dependent on N form. The medium was acidified under ammoniacal regime and alkalinized under nitric regime regardless of Fe level. FCR activity stimulation in response to Fe deficiency was observed only in NO 3- fed plants. In addition, both N form and Fe level induced antioxidant responses in rosette leaves. Ammoniacal regime increased both peroxidase expression and anthocyanin accumulation, whereas Fe deficiency enhanced superoxide dismutase expression.
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PMID:Physiological responses of Arabidopsis thaliana to the interaction of iron deficiency and nitrogen form. 2051 74


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