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

Severe iron deficiency was induced in rats by rearing nursing dams and their offspring on a diet comprising all the requisite nutrients and trace metals except iron. The iron deficient 5-week-old rats exhibited a severe anemia and a drastic decrease in iron content of the hepatic tissue and of the mitochondrial fraction. Cytochromes c + c1 and b were moderately but significantly reduced. A large increase in liver concentration was observed in iron-deficient animals; whereas there was no modification in total lipid, cholesterol, phospholipid and fatty acid composition of the mitochondrial membrane. Mitochondria from iron-deficient rats presented a partial uncoupling of the oxidative phosphorylation process. This functional derangement was completely reversed by the presence of either bovine serum albumin or L-carnitine plus ATP. This behaviour suggested that endogenous long-chain fatty acids could be primarily involved in the onset of mitochondrial dysfunction. The hepatic energy state of the liver appeared dramatically decreased under the pathological condition of severe iron-deficiency anemia. The possibility of a direct link between the partial loss of coupled functions observed in isolated mitochondria and the heavy energy deficit detected in the liver is discussed.
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PMID:Dietary iron deficiency in the rat. I. Abnormalities in energy metabolism of the hepatic tissue. 794 4

Chronic exposure of adult rats to dietary intake of cadmium (15 mg CdCl2/day/kg for 30 days) leads to development of anemia and thrombocytosis. Anemia is characterized by significant reticulocytosis (13.1 +/- 1.0%), anysocytosis, poikilocytosis, iron deficiency and marked alterations of antioxidant and metabolic status of red blood cells. Activities of SOD, catalase, GPx and GR were significantly increased in red blood cells of cadmium-treated rats. In treated animals cadmium induced an increase of red cell reduced and oxidized glutathione with no changes of GSSG/GSH ratio. However, significant reduction of lipid peroxidation was found. Plasma levels of tocopherol and ascorbate, as well as activity of glutathione-S-transferase, were all significantly increased in cadmium-treated rats. The energy metabolism of red blood cells was deeply altered in cadmium-treated rats. The levels of ATP, ADP, AMP and TAN were significantly increased while ATP/ADP ratio and adenylate energy charge (AEC) were significantly reduced. The level of 2,3-BPG was somewhat lower, but 2,3-BPG/Hb ratio was considerably higher, in red blood cells of cadmium-treated rats.
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PMID:Cadmium-induced changes of antioxidant and metabolic status in red blood cells of rats: in vivo effects. 837 Apr 23

Using 31P magnetic resonance spectroscopy we compared skeletal muscle bioenergetics in Wistar rats made chronically anaemic by being fed a diet deficient in iron for 6 weeks with chronically iron deficient animals given a normal diet as well as 5 mg iron dextran at 2 or 7 days before experimentation. Spectra of the gastrocnemius muscle were taken at rest and during stimulation of the sciatic nerve at 2 Hz for 10 min. Relative concentrations of intracellular phosphate (Pi), phosphocreatine (PCr) and ATP were determined. Iron deficiency increased PCr breakdown and production of acid in stimulated skeletal muscle. Recovery of PCr and Pi concentrations after exercise was slow. These metabolic changes are consistent with either a reduction in supply of oxygen to the muscle cell or altered oxidative phosphorylation by the mitochondria. The latter may be mediated by defective function of iron-containing proteins crucial in oxidative phosphorylation and this is suggested both by the observation that treatment with iron, sufficient to correct the anaemia, does not completely reverse the metabolic changes and that there is a different time course for such metabolic improvements and the observed increase in haemoglobin concentration.
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PMID:The effect of iron deficiency on skeletal muscle metabolism of the rat. 845 45

Iron regulatory protein 1 (IRP1) and IRP2 are cytoplasmic RNA binding proteins that are central regulators of mammalian iron homeostasis. We investigated the time-dependent effect of dietary iron deficiency on liver IRP activity in relation to the abundance of ferritin and the iron-sulfur protein mitochondrial aconitase (m-acon), which are targets of IRP action. Rats were fed a diet containing 2 or 34 mg iron/kg diet for 1-28 d. Liver IRP activity increased rapidly in rats fed the iron-deficient diet with IRP1 stimulated by d 1 and IRP2 by d 2. The maximal activation of IRP2 was five-fold (d 7) and three-fold (d 4) for IRP1. By d 4, liver ferritin subunits were undetectable and m-acon abundance eventually fell by 50% (P < 0.05) in iron-deficient rats. m-Acon abundance declined most rapidly from d 1 to 11 and in a manner that was suggestive of a cause and effect type of relationship between IRP activity and m-acon abundance. In liver, iron deficiency did not decrease the activity of cytosolic aconitase, catalase or complex I of the electron transport chain nor was there an effect on the maximal rate of mitochondrial oxygen consumption with the use of malate and pyruvate as substrates. Thus, the decline in m-acon abundance in iron deficiency is not reflective of a global decrease in liver iron-sulfur proteins nor does it appear to limit ATP production. Our results suggest a novel role for m-acon in cellular iron metabolism. We conclude that, in liver, iron deficiency preferentially affects the activities of IRPs and the targets of IRP action.
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PMID:Dietary iron intake rapidly influences iron regulatory proteins, ferritin subunits and mitochondrial aconitase in rat liver. 948 59

Various biochemical and biophysical studies have demonstrated the existence of a novel iron-uptake mechanism in Pseudomonas aeruginosa, different from that generally described for ferrichrome and ferric-enterobactin in Escherichia coli. This new iron-uptake mechanism involves all the proteins generally reported to be involved in the uptake of ferric-siderophore complexes in Gram-negative bacteria (i.e. the outer membrane receptor, periplasmic binding protein and ATP-binding-cassette transporter), but differs in the behaviour of the siderophore. One of the key features of this process is the binding of iron-free pyoverdin to the outer membrane receptor FpvA in conditions of iron deficiency.
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PMID:A new mechanism for membrane iron transport in Pseudomonas aeruginosa. 1219 69

The effects of iron deficiency on cell culture growth, cell respiration, mitochondrial oxidative properties, and the electron transport chain were studied with suspension-cultured sycamore (Acer pseudoplatanus L.) cells. Iron deprivation considerably decreased the initial growth rates and limited the maximum density of the cells. Under these conditions, the cells remained swollen throughout their growth. The absence of iron led to a steady decline in the uncoupled rate of O2 consumption. When the uncoupled rate of O2 uptake closely approximated the respiratory rate, the cells began to collapse. At this stage, the level of all the cytochromes and electron paramagnetic resonance-detectable Fe-S clusters of the mitochondrial inner membrane were dramatically decreased. Nevertheless, it appeared from substrate oxidation measurements that this overall depletion in iron-containing components solely disturbed the functioning of complex II, whereas neither complexes I, III, or IV, nor the machinery involved in ATP synthesis, was apparently impaired in iron-deficient mitochondria. However, our results suggest that the impairment of complex II resulted in a strong reduction of the overall capacity of the mitochondrial electron transport chain, which was responsible for determining the rate of endogenous respiration in sycamore cells. Finally, this situation led to a depletion of various energy metabolites that could contribute to the premature cell death.
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PMID:Effect of Iron Deficiency on the Respiration of Sycamore (Acer pseudoplatanus L.) Cells. 1223 26

To learn more about the adaptive response of Synechococcus elongatus PCC 7942 to iron starvation and the role of DpsA, presumably a protein protecting chromosomal DNA against oxidative damage, we performed a comparative analysis of S. elongatus PCC 7942 wild-type and a DpsA-free mutant, called K11. Relative to wild-type, the DpsA-free mutant had significantly higher amounts of phycocyanin and allophycocyanin, even upon iron limitation. While the Photosystem I activity in mutant K11 remained high under iron deficiency, the Photosystem II activity dropped severely with respect to wild-type. The DpsA content in wild-type was already fairly high under regular growth conditions and did not significantly increase under iron deficiency nor in the presence of 0.3 mM 2'2'-dipyridyl in iron-sufficient BG11 medium. Nevertheless, the absence of DpsA in K11 resulted in a significantly altered transcriptional/translational activity of genes known to be involved in adaptation to iron starvation. The amount of isiA/B transcript was about two-fold lower than in wild-type, resulting in a lower 77 K chlorophyll a fluorescence at 685 nm, implying a lower concentration of Photosystem I-IsiA supercomplexes. While in wild-type idiA, idiB, and irpA transcripts were highly up-regulated, hardly any were detectable in mutant K11 under iron limitation. The concentration of mapA transcript, however, was greatly increased in K11 compared to wild-type. Measurements of acridine yellow fluorescence with intact wild-type and K11 cells revealed that iron deficiency caused an increased contribution of cyclic electron transport to membrane energisation and ATP synthesis being in agreement with the formation of the Photosystem I-IsiA supercomplex. In addition, mutant K11 had a much higher respiratory activity compared to wild-type under iron limitation.
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PMID:Adaptation to iron deficiency: a comparison between the cyanobacterium Synechococcus elongatus PCC 7942 wild-type and a DpsA-free mutant. 1624 95

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

Gas exchange and chlorophyll a fluorescence in soybean plants were investigated to explore the effects of iron deficiency on photosynthesis and photosystem II function in vivo. Iron deficiency induced a drastic decrease in net photosynthesis (Pn). Compared with normal plants, the maximal quantum yield of PSII photochemistry (psipo) in iron-deficient plants was only slightly lower; whereas, the efficiency with which a trapped exciton can move an electron into the electron transport chain further than QA-(Psio) and quantum yield of electron transport beyond QA (psiEo) were significantly depressed. Iron deficiency also caused a clear enhancement of the relative variable fluorescence at K step (VK). When exposed to light, iron-deficient plants had considerably lower efficiency of excitation energy capture by open PSII reaction centers (Fv'/Fm'), quantum yield of PSII electron transport (PhiPSII), and photochemical quenching coefficient (qP), but markedly higher non-photochemical quenching (NPQ). In addition, post-illumination transient increase in chlorophyll fluorescence was clearly enhanced in iron-deficient plants. Basing on these data, we suggest that both the donor and the acceptor sides of PSII complex were damaged by iron deficiency; cyclic electron transport around PSI in iron-deficient soybean plants might play an important role in inducing the excitation energy dissipation and meeting the demand for extra ATP as a compensation for the loss of phosphorylation capability.
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PMID:Effects of iron deficiency on photosynthesis and photosystem II function in soybean leaf. 1728 70

To know the root adjustment in response to iron deficiency, differentially displayed proteins in tomato roots of wild type and its iron uptake inefficient mutant T3238fer were analyzed by 2-DE and MALDI-TOF MS-based proteomic method under iron sufficiency and deficiency. Ninety-seven proteins were identified, 63 of them were classified in various metabolic pathways. About 40 proteins involved in starch degradation, TCA and ascorbate cycles were upregulated under iron deficiency and grouped in a network together with glycolysis, whereas proteins for fructose metabolism were decreased. Proteins involved in methionine synthesis, cell wall synthesis, mitochondria ATP synthesis, vacuole ATPase, HSP70/90, etc. also revealed enhanced expression under iron deficiency, while proteins about redox homeostasis, transcription factors, kinases, etc. showed diversified changes. The responses are closely associated with energy metabolism, organic acid formation, root morphological change, redox and sulfur homeostasis, and signal transduction, which enhance iron uptake, reutilization and other adaptive changes. Most of the proteins affected by iron deficiency and fer mutation showed similar effect on individual proteins or pathways, but the independent function of FER to iron deficiency were statistically indicated.
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PMID:Proteomic response to iron deficiency in tomato root. 1845 29


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