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

This study gave us the opportunity to know the roles iron deficiency and the presence of lead in blood play, as confounding variables, in relation to the state of malnutrition and the intellect of those children. A sample of 169 school children were classified according to their state of nutrition, their condition in reference to serum iron and lead concentrations. In addition, their intelligence was evaluated. The results confirmed that those children with lower weights and heights registered lesser points of intelligence; in fact, iron deficiency cancels out the difference in favor of those taller and weighing more. Lead did not contribute as a confounding variable, but more than half of the children showed possible toxic levels of this metal.
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PMID:[The intelligence quotient and malnutrition. Iron deficiency and the lead concentration as confusing variables]. 176 60

Lead administration (250, 500, 1000, and 2000 ppm, as lead acetate) in drinking water during fetal development (from 15 to 20 days of gestation), in normal and iron-deficient pregnant rats, revealed dose-dependent increases in the lead content of maternal blood that was more marked in iron-deficient animals. The placentae and fetuses did not show a dose-dependent increase in lead content. Lead administration revealed dose-dependent hydropic degeneration of renal proximal cells in the fetuses. The highest dose (2000 ppm lead) and iron deficiency exhibited more lead accumulation in maternal blood, placentae, and fetuses, and maximum pathologic changes in the fetal kidney when compared with the other doses and also with the fetuses of dams not deficient in iron.
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PMID:Lead-induced fetal nephrotoxicity in iron-deficient rats. 180 55

A blood lead survey was conducted on samples from 2459 children aged 3-6 years to determine the prevalence of lead poisoning in children of this age in the Province of Ontario. Lead poisoning, defined as a blood lead concentration greater than or equal to 1.21 mumol 1-1 (25 micrograms dl-1), was found in 26 subjects (1.1% of the samples). The mean blood lead concentration for children from southern Ontario was 0.50 mumol l-1, and for those from northern Ontario it was 0.37 mumol l-1. Stringent quality controls and independent cross-checks of finger-prick capillary blood sampling were employed in the study. The free erythrocyte protoporphyrin levels were also monitored to detect the presence of iron deficiency in the children.
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PMID:Blood lead screening in Ontario children: blood lead and free erythrocyte protoporphyrin levels. 261 89

Concern for the concomitant occurrence of iron deficiency and elevated blood lead in children is raised by animal studies documenting increased gastrointestinal lead absorption in the presence of iron deficiency. An elevation in free erythrocyte protoporphyrin (FEP) above 35 mg/dl is seen with both iron deficiency and lead toxicity. To determine whether the degree of elevation in FEP is useful in predicting which children with elevated blood lead levels have concomitant iron deficiency, 109 children suspected of having an elevated lead burden were studied. A complete blood count, reticulocyte count, FEP, lead, and ferritin were measured on each child. The effect of the independent variables, lead and iron status, both alone and in combination, on the dependent variable, FEP, was analyzed through a linear regression model. Lead status alone accounted for 42 percent of the explained variance in FEP, and the lead-iron interaction increased the explained variance by only an additional 1 percent. Screening for iron deficiency in children with elevated blood lead should continue to be based on dietary and socioeconomic risk factors and not on degree of elevation in FEP.
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PMID:Combined iron deficiency and lead poisoning in children. Effect on FEP levels. 367 34

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

Iron deficiency and lead toxicity both result in increased erythrocyte protoporphyrin. The purpose of this study was to determine the differences in EP concentration, according to age and sex, obtained in the 2nd National Health and Nutrition Examination Survey of the United States and to determine the extent to which EP differences might be related to iron deficiency or lead toxicity. The highest EP concentrations were found in infants and children. Among adults, women had higher EP values than men. Lead toxicity (blood lead greater than 30 micrograms/dl) and low serum iron concentration/total iron binding capacity (Fe/TIBC less than 16%), often in combination, were associated with elevated EP values in infants and children. In women, elevated EP concentration were related primarily to low Fe/TIBC values, whereas in men there was only a weak association with elevated blood lead concentration. Age/sex differences in EP values diminished markedly when the influences of lead toxicity and iron deficiency were excluded by the above criteria.
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PMID:Developmental changes in erythrocyte protoporphyrin: roles of iron deficiency and lead toxicity. 671 18

Lead, cadmium, and mercury are toxic metals that are not essential for nutrition. However, the toxic effects of these metals may be mediated or enhanced by interactions or deficiencies of nutritionally essential metals. Lead competes with calcium, inhibiting the release of neurotransmitters, and interferes with the regulation of cell metabolism by binding to second-messenger calcium receptors, blocking calcium transport by calcium channels and calcium-sodium ATP pumps, and by competing for calcium-binding protein sites and uptake by mitochondria. Dietary deficiencies of calcium, iron, and zinc enhance the effects of lead on cognitive and behavioral development. Iron deficiency increases the gastrointestinal absorption of cadmium, and cadmium competes with zinc for binding sites on metallothionein, which is important in the storage and transport of zinc during development. Selenium protects from mercury and methyl mercury toxicity by preventing damage from free radicals or by forming inactive selenium mercury complexes.
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PMID:Nutrition and metal toxicity. 787 32

Environmental lead intoxication, which frequently causes neurological disturbances, and iron deficiency are clinical problems commonly found in children. Also, iron deficiency has been shown to augment lead absorption from the intestine. Hence, there is evidence for an interaction between lead and iron metabolism which could produce changes in lead and iron uptake by the brain and other tissues. These possibilities were investigated using 15-, 21-, and 63-old rats with varying nutritional iron and lead status. Dams were fed diets containing 0 or 3% lead-acetate and 0.2% lead-acetate in the drinking water. After weaning, 0.2% lead-acetate in the drinking water became the sole source of dietary lead. Measurements were made of tissue lead and nonheme iron levels and the uptake of 59Fe after intravenous injection of transferrin-bound 59Fe. Iron deficiency was associated with increased intestinal absorption of lead as indicated by blood and kidney lead levels in rats exposed to dietary lead. However, iron deficiency did not increase lead deposition in the brain, and in all rats brain lead levels were relatively low (< 0.1 microgram/g). Lead concentrations in the liver were below 2 micrograms/g, whereas kidneys had almost 20 times this concentration. Animals with iron deficiency had lower liver iron levels and had increased brain 59Fe uptake in comparison to control rats. However, iron levels in brain and kidneys were unaffected by lead intoxication regardless of the animal's iron status. 59Fe uptake rates were also unaffected by lead, but increased rates of uptake were apparent in iron-deficient rats. Lead did increase liver iron levels in all iron-adequate rats, but iron deficiency had little effect. It is concluded that, compared with other tissues, the blood-brain barrier largely restricts lead uptake by the brain and that the uptake that does occur is unrelated to the iron status of the animal. Also, the level of lead intoxication produced in this investigation did not influence iron uptake by the brain and kidneys, but liver iron stores could be increased if iron levels were already adequate.
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PMID:Interactions between tissue uptake of lead and iron in normal and iron-deficient rats during development. 881 Dec 82

Cadmium, lead, mercury, and aluminum are toxic metals that may interact metabolically with nutritionally essential metals. Iron deficiency increases absorption of cadmium, lead, and aluminum. Lead interacts with calcium in the nervous system to impair cognitive development. Cadmium and aluminum interact with calcium in the skeletal system to produce osteodystrophies. Lead replaces zinc on heme enzymes and cadmium replaces zinc on metallothionein. Selenium protects from mercury and methylmercury toxicity. Aluminum interacts with calcium in bone and kidneys, resulting in aluminum osteodystrophy. Calcium deficiency along with low dietary magnesium may contribute to aluminum-induced degenerative nervous disease.
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PMID:Toxic and essential metal interactions. 924 Sep 18

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


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