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

Daily intraperitoneal administration of manganese chloride (15 mg/kg) to rats, maintained on an irondeficient diet, produced marked alterations in the activity of succinic dehydrogenase, monoamine oxidase, and in the morphology of the liver. Manganese accumulation was also significantly increased in such rats than after similar treatment to normally fed rats. Iron deficiency leads to increased absorption of manganese which is responsible for increased susceptibility to manganese toxicity in these animals.
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PMID:Role of iron deficiency in inducing susceptibility to manganese toxicity. 98 99

Metals such as lead, zinc, copper, aluminum and manganese have been implicated in neuropsychiatric disorders. However, until fairly recently the role of iron in brain function was rather obscure, because little attention was paid to its metabolism in the brain. It is now apparent that maintenance of brain iron homoeostasis is important for the normal functioning of his organ. Most of the studies have been directed towards the cognitive and attentional deficit resulting from nutritional iron deficiency. Evidence so far suggests subsensitivity of striatal dopamine neurotransmission. By contrast the selective increase in free iron in the substantia nigra pars compacta of parkinsonian brains is thought to initiate oxidative stress, from iron-induced liberation of cytotoxic oxygen free radicals. Such radicals are known to promote membrane fluidity, alteration in cellular calcium homoeostasis, lipid peroxidation and finally cell death in systemic organs. Evidence supporting similar processes being responsible for nigrostriatal dopamine neuron degeneration in Parkinson's disease is now becoming available. Such possibilities afford the development of neuroprotective drugs as a means to retard the progression of this disorder. These include other selective monoamine oxidase B inhibitors, iron chelators with the ability to cross the blood-brain barrier, selective calcium channel antagonists and mitochondrial electron transport system protectors.
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PMID:Iron in brain function and dysfunction with emphasis on Parkinson's disease. 164 57

To clarify the influence of iron deficiency on mineral status, the following two synthetic diets were fed to male Wistar rats: a control diet containing 128 micrograms iron/g, and an iron-deficient diet containing 5.9 micrograms iron/g. The rats fed the iron-deficient diet showed pale red conjunctiva and less reactiveness than the rats fed the control diet. The hemoglobin concentration and hematocrit of the rats fed the iron-deficient diet were markedly less than the rats fed the control diet. The changes of mineral concentrations observed in tissues of the rats fed the iron-deficient diet, as compared with the rats fed the control diet, are summarized as follows: . Iron concentrations in blood, brain, lung, heart, liver, spleen, kidney, testis, femoral muscle, and tibia decreased; . Calcium concentrations in blood and liver increased; calcium concentration in lung decreased; . Magnesium concentration in blood increased; . Copper concentrations in blood, liver, spleen and tibia increased; copper concentration in femoral muscle decreased; . Zinc concentration in blood decreased; . Manganese concentrations in brain, heart, kidney, testis, femoral muscle and tibia increased. These results suggest that iron deficiency affects mineral status (iron, calcium, magnesium, copper, zinc, and manganese) in rats.
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PMID:Effect of dietary iron deficiency on mineral levels in tissues of rats. 172 8

Seven different metals (iron, copper, zinc, calcium, manganese, lead, and cadmium) were studied in eight different brain regions (cerebral cortex, cerebellum, corpus striatum, hypothalamus, hippocampus, midbrain, medulla oblongata, and pons) of weaned rats (21-d-old) maintained on an iron-deficient (18-20 mg iron/kg) diet for 8 wk. Iron was found to decrease in all the brain regions, except medulla oblongata and pons, in comparison to their respective levels in control rats, receiving an iron-sufficient (390 mg iron/kg) diet. Brain regions showed different susceptibility toward iron deficiency-induced alterations in the levels of various metals, such as zinc, was found to increase in hippocampus (19%, p less than 0.05) and midbrain (16%, p less than 0.05), copper in cerebral cortex (18%, p less than 0.05) and corpus striatum (16% p less than 0.05), calcium in corpus striatum (22%, p less than 0.01) and hypothalamus (17%, p less than 0.02), and manganese in hypothalamus (18%, p less than 0.05) only. Toxic metals lead and cadmium also increased in cerebellum (19%, p less than 0.05) and hippocampus (17%, p less than 0.05) regions, respectively. Apart from these changes, liver (64%, p less than 0.001) and brain (19%, p less than 0.01) nonheme iron contents were found to decrease significantly, but body, liver, and brain weights, packed cell volume, and hemoglobin content remained unaltered in these experimental rats. Rehabilitation of iron-deficient rats with an iron-sufficient diet for 2 wk recovered the values of zinc in both the hippocampus and mid-brain regions and calcium in the hypothalamus region only. Liver nonheme iron improved significantly; however, no remarkable effect was noticed in brain nonheme iron following rehabilitation. It may be concluded that latent iron deficiency produced alterations in various metal levels in different brain regions, and corpus striatum was found to be the most vulnerable region for such changes. It is also evident that brain regions were resistant for any recovery in their altered metallic levels in response to rehabilitation for 2 wk.
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PMID:Effect of latent iron deficiency on metal levels of rat brain regions. 248 35

Day-old Japanese quail were fed purified diets containing either 0.2 (control), 5.4, or 16.2 ppm lead as the acetate with either 25 (deficient) or 100 ppm (adequate control) iron for 2 weeks. Iron deficiency caused decreases in hemoglobin, iron, and manganese in the liver, and hepatic RNA synthesis. Iron deficiency also caused increased concentrations of lead, calcium, and molybdenum in the liver. Lead supplements caused increased concentrations of lead in the liver, and with adequate dietary iron, each supplemental lead level caused a slight decrease in the concentration of RNA in the liver. Treatment had no effect on DNA or protein synthesis, body weight, or liver weight in relation to body weight. These low levels of dietary lead did not cause the same adverse metabolic effects observed by others with higher levels of lead; however, iron deficiency increased lead uptake by the liver and affected RNA synthesis.
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PMID:Effects of low levels of dietary lead and iron on hepatic RNA, protein, and minerals in young Japanese quail. 620 50

Methylcyclopentadienyl manganese tricarbonyl (MMT) is effective in raising the octane level of gasoline and is currently used in Canada for that purpose in a maximal concentration of 18 mg Mn/l (slightly less than 0.07 g Mn/U.S. gal). It has been estimated that if MMT were used in all U.S. gasoline in these amounts, the median increase of Mn in ambient air would be not more than 0.05 microgram Mn/m3, with increments generally less than 0.5 microgram Mn/m3 along urban corridors. The scientific literature was reviewed to determine how the increases in environmental manganese predicted from MMT use would relate to the amounts in the natural environment and necessary to life and to the concentrations associated with toxic effects. Even with additional manganese from the use of fuel additives, total Mn intakes would remain within the range of average amounts absorbed from food and water. Respirable manganese in ambient air due to MMT combustion would be many order of magnitude below the concentrations associated with occupational manganism and respiratory problems and also below those reported in isolated episodes of respiratory symptoms in communities near ferromanganese plants. Evidence was reviewed on the possibilities of: (1) increased absorption of inhaled manganese compared with ingested manganese; (2) hypersusceptibility of infants and persons of advanced age; and (3) increased absorption associated with iron deficiency. While relevant to high levels of exposure, these factors would not be expected to lead to toxic effects from the very low concentrations of Mn resulting from MMT use. Experimental animals that inhaled the combustion products of MMT in concentrations of approximately 10, 100, and 1000 micrograms Mn/m3 for 9 mo did not show toxic effects, although there was temporary elevation of tissue levels of Mn. Rhesus monkeys, susceptible to the neurologic effects of Mn, showed no symptoms after inhaling the combustion products of MMT in concentrations of 100 micrograms Mn/m3 for up to 66 wk. Monkeys exposed to 5000 microgram Mn/m3 also showed no symptoms. There is thus a wide margin of safety between the intakes of Mn essential to health and the high concentrations that have been associated with toxic effects. The small amounts of manganese added to the environment by the combustion of MMT used as a fuel additive would be comparable to the normal background and should not create health problems.
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PMID:The health implications of increased manganese in the environment resulting from the combustion of fuel additives: a review of the literature. 638 93

Dietary iron deficiency enhances the absorption of iron, cobalt, manganese, zinc, cadmium and lead, whereas, iron deficiency due to bleeding increases the absorption of iron, cobalt and perhaps manganese. To determine whether the response to bleeding is qualitatively different from that induced by dietary iron deficiency, metal absorption was studied in mice fed either a high-iron diet (120 ppm Fe) and bled (0.5 ml) or fed a low-iron diet (< 3 ppm Fe). Iron absorption from an intragastric dose was increased by the loss of 0.5 ml of blood; smaller losses of blood had no effect. Also, iron absorption was increased more by dietary iron deficiency than by bleeding. In perfusion experiments, bleeding increased the duodenal absorption of only iron and cobalt, whereas dietary iron deficiency enhanced the absorption of all the metals except cadmium. The patterns of absorptive inhibition of the metals by each other were similar in bled mice and in mice with dietary iron deficiency except that interactions among metals with lower affinities for the iron absorption mechanism--manganese, zinc, cadmium and lead--were more obvious in mice fed the low-iron diet. We concluded that bleeding only partially activates the iron absorptive mechanism and that the lack of a bleeding effect on the absorption of manganese, zinc, cadmium and lead results from the weaker interactions of these metals, with a partly-activated absorption process.
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PMID:Comparative effects of iron deficiency induced by bleeding and a low-iron diet on the intestinal absorptive interactions of iron, cobalt, manganese, zinc, lead and cadmium. 741 Dec 35

Rats (Wistar, female, 4 weeks old) were fed iron-deficient (Fe-; 2.2 micrograms Fe/g) or manganese- and copper-deficient (Mn.Cu-; 0.3 microgram Mn/g, 0.4 microgram Cu/g) diets for 8 weeks to determine the oxidative damage of DNA by element deficiency. After feeding of the diets, 2-nitropropane (2-NP, 80 mg/kg body weight) was administered i.p. as an inducer of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) to the element-deficient rats. The hemoglobin concentration of rats in the Fe- group showed an induction of severe anemia (8.4 g/100 ml whole blood). In the Mn.Cu- group, Mn-superoxide dismutase (SOD) activities of plasma and Cu.Zn-SOD activities were significantly lower than that of the normal diet group. However, total SOD activities of plasma were not depressed severely in contrast to that of the liver in the Mn.Cu- group. Background (spontaneous) levels of 8-OH-dG in normal diet group were 0.96 +/- 0.37/10(5) deoxyguanosine (dG), however, significantly higher levels were detected in the Fe- group (1.56 +/- 0.19, P < 0.01). Conversely, a lower (but not significant) level of 8-OH-dG than the normal diet group were detected in the Mn.Cu- group (0.78 +/- 0.08). Six hours after 2-NP treatment, 8-OH-dG levels in liver DNA were significantly induced to 1.44 +/- 0.24 in the normal diet fed group 1.89 +/- 0.22 in the Fe- and 1.08 +/- 0.12 in the Mn.Cu- groups. Compared to the normal diet group, these induced levels of 8-OH-dG in the Fe- group were significantly higher (P < 0.05), and that in Mn.Cu- group were significantly lower (P < 0.05). The high level of 8-OH-dG in severe iron deficiency might be the results of: (i) an increase of hydroxyl radical generation by accumulated copper in hepatocytes; or (ii), a depression of enzymatic activity for removing 8-hydroxy-2'-deoxyguanosine in DNA, which is dependent on divalent cations. On the other hand, the low level of 8-OH-dG in manganese and copper deficiency might be the result of a decrease of lipid peroxidation which has been suggested to be an intermediator from active oxygen species to hydroxyl radical.
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PMID:Spontaneous and 2-nitropropane induced levels of 8-hydroxy-2'-deoxyguanosine in liver DNA of rats fed iron-deficient or manganese- and copper-deficient diets. 838 15

Metal ions are essential cofactors for a wealth of biological processes, including oxidative phosphorylation, gene regulation and free-radical homeostasis. Failure to maintain appropriate levels of metal ions in humans is a feature of hereditary haemochromatosis, disorders of metal-ion deficiency, and certain neurodegenerative diseases. Despite their pivotal physiological roles, however, there is no molecular information on how metal ions are actively absorbed by mammalian cells. We have now identified a new metal-ion transporter in the rat, DCT1, which has an unusually broad substrate range that includes Fe2+, Zn2+, Mn2+, Co2+, Cd2+, Cu2+, Ni2+ and Pb2+. DCT1 mediates active transport that is proton-coupled and depends on the cell membrane potential. It is a 561-amino-acid protein with 12 putative membrane-spanning domains and is ubiquitously expressed, most notably in the proximal duodenum. DCT1 is upregulated by dietary iron deficiency, and may represent a key mediator of intestinal iron absorption. DCT1 is a member of the 'natural-resistance-associated macrophage protein' (Nramp) family and thus its properties provide insight into how these proteins confer resistance to pathogens.
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PMID:Cloning and characterization of a mammalian proton-coupled metal-ion transporter. 924 8

This article examines the evolution of nutritional iron deficiency and the possible interactions with other minerals, such as manganese, in control and iron-deficient rats. The evolution of iron deficiency was studied at 0, 10, 20, 30 and 40 days of providing the animals with an iron-free diet (diet 0). It was found that the critical period in the development of nutritional iron deficiency occurs after 30-40 days without iron, at which moment the organism is unable to maintain hemoglobin levels without endangering the iron-dependent enzymatic groups which, in turn, are essential for life. It was also demonstrated that in a situation of iron deficiency, there occurs a greater absorption of manganese. It should be noted that this greater absorption of manganese is not reflected in the concentration of the mineral in the organs. Therefore, it is evident that the interactions of iron with manganese take place at the digestive level with no apparent consequences being observed at the metabolic level.
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PMID:Iron-manganese interactions in the evolution of iron deficiency. 962 80


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