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

Relationships between various types of chronic anemia, wound healing, and red cell 2,3-diphosphoglycerate (2,3 DPG) were examined in rabbits. Wound tensile strength and energy absorption were not affected by chronic iron-deficiency anemia, the chronic hemolytic anemia caused by intravenous water infusion nor by chronic hemolytic anemia caused by intravenous water infusion nor by chronic phenylhydrazine-induced anemia. Red cell 2,3 DPG levels were increased in the anemia of iron deficiency and were normal in the rabbits with chronic phenylhydrazine-induced anemia at the time of wound excision but were low following phynylhydrazine injection. The results show that chronic anemia per se does not affect the tensile strength and energy adsorption of wound healing. The findings suggest that the wound healing process may differ in certain types of anemia.
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PMID:Chronic anemia, wound healing, and red cell 2,3-diphosphoglycerate. 0 66

By an improved isolation procedure chloroplasts could be obtained from the alga Bumilleriopsis filiformis (Xanthophyceae) which exhibited high electron transport rates tightly coupled to ATP formation. Uncouplers both stimulate electron transport and inhibit photophosphorylation. These chloroplasts retain almost all soluble cytochrome c-553 besides a membrane-bound cytochrome c-554.5 (=f-554.5). Sonification or iron deficiency removed the soluble cytochrome only with a concurrent decrease of electron transport from water to methyl viologen or to NADP and decreased non-cyclic and cyclic photophosphorylation. However, photosynthetic control and the P/2e ratios remain unaltered. In Bumilleriopsis, which apparently has no plastocyanin, the soluble cytochrome c-553 seemingly links electron transport between the bound cytochrome c and P-700.
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PMID:The role of plastidic cytochrome c in algal electron transport and photophosphorylation. 20 17

The aim of this investigation was to establish the relationship of cadmium-induced fetal growth retardation in the mouse to iron deficiency. Pregnant mice were either fed a low iron diet or given 40 ppm cadmium in their drinking water. The effects of these factors on fetal weight and hematological values of the fetuses and dams were established and compared, both with each other and with appropriate controls. Both treatments caused maternal and fetal anemia, the fetuses being more severely affected. The anemic fetuses were also severely growth retarded. These changes, when caused by the iron deficient diet, could be completely prevented by either parenterally or orally administered iron supplements. When the changes were caused by cadmium in the drinking water they were only partially prevented by oral supplements. From these results it was concluded that iron deficiency in pregnancy causes not only anemia but also fetal growth retardation. Cadmium exposure in pregnancy, presumably by blocking intestinal absorption of iron, also causes anemia and hence fetal growth retardation.
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PMID:Iron deficiency and its role in cadmium-induced fetal growth retardation. 47 57

Two experiments are reported which show that rats are capable of forming an association between the presence of iron in a solution when it is not specifically needed and a subsequent state of iron deficiency. Specifically, rats were trained to lever press for water while thirsty. One group received ferrous ions in addition to the water. When these rats were subsequently rendered iron deficient, they lever pressed more under extinction conditions as a graded function of lower hemoglobin levels. Controls that either did not receive ferrous ions during training or received solutions other than ferrous solutions during training did not respond this way under extinction conditions. This is therefore a type of latent learning previously demonstrated only for sodium appetite.
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PMID:Iron appetite and latent learning in rats. 61 94

In mice fed a low iron diet, the addition of low levels of cadmium chloride (10 micrometer) to the drinking water impaired growth and accentuated the development of anemia. Cadmium had no effect on mice given a similar diet supplemented with iron. Iron deficiency increased the concentration of cadmium in the duodenal mucosa, the transfer of cadmium to the body from the intestinal tract, and the deposition of absorbed cadmium in the kidneys. In human subjects, the average absorption of 25 microgram of cadmium, labeled with 115mCd, from a test meal was 8.9 +/- 2.0% (mean +/- SE) in 10 people with low body iron stores (serum ferritin less than 20 ng per ml) and 2.3 +/- 0.3% in 12 subjects with normal iron stores (serum ferritin greater than 23 ng per ml). The biological half-time of the radiocadmium in 3 of the subjects ranged from 90 to 202 days. Thus, the intestinal adaptive response to iron deficiency in both experimental animals and human subjects leads to the increased absorption of cadmium, a potentially toxic element.
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PMID:Increased dietary cadmium absorption in mice and human subjects with iron deficiency. 64 Mar 39

A classification of formulas with defined compositions of their nutritive substances into 3 groups has been made in the Federal Republic of Germany with the objective to achieve a standardization. It is differentiated between adapted, partially adapted, and non-adapted formulas. As defined, the composition of adapted formulas is closest to human milk. Since adapted formulas are thought to be of physiological value, one is surprised by the fact, that shortly after discharge from the maternity hospital partially adapted or nonadapted formulas are favoured by a high percentage (of mothers). The reasons for this are analyzed. By the end of the third month of life the premature infant is depending on the administration of iron. At this time signs of a more or less latent iron deficiency are developing. In the full term infant this condition will be reached approximately by the age of six months. Since iron-salts may interfere with the vitamin E supply in the premature infant, one should either administer a water soluble vitamin E preparation or the necessary iron prophylaxis should be started in these children only in the third month of life.
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PMID:[New aspects of the feeding of the newborn and young infant (author's transl)]. 125 Jun 33

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

It is hypothesized that electric shock can compensate for the learning deficit caused by iron deficiency in the experimental rat population, and that this effect will be sustained over a 3-week "rehabilitation" period. Forty-seven female Sprague-Dawley rats served as the experimental subjects. The learning capacity of the rats was assessed using a water Y-maze. The dependent variables were assessed twice, once after half had been made iron deficient, and again after the iron deficiency had been corrected. A 2 x 2 x 2 analysis of variance with repeated measures was employed, along with post-hoc tests, to assess the effects of the experimental manipulations on the rats' performance. The experimental results replicated previous findings regarding the damaging effects of iron deficiency on learning capacity in rats and confirmed that shock improves the performance of rats in the water Y-maze. Furthermore, it was found that shock and iron deficiency interact, such that the performance of iron-deficient rats subjected to electric shock is superior to that of rats not made iron deficient. This trend persists even after the hematological effects of iron deficiency are corrected, although to a less dramatic degree. A possible explanation for these findings is advanced.
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PMID:The effects of iron deficiency and electric shock on learning in rats. 193 58

Almost all segments of the gastrointestinal tract have been used as urinary tract substitutes. The specific nutritional and gastrointestinal complications depend on the particular portion of bowel that is removed from the alimentary tract. The use of stomach theoretically may predispose the patient to hypergastrinemia and peptic ulcer disease, hypocalcemia, and iron deficiency or megaloblastic anemia. Resection of a large amount of jejunum causes malabsorption. Limited use of colon segments usually is well tolerated, but loss of large parts of the colon directly decreases available absorptive area, resulting in diarrhea. Resection of the ileum and ileocecal valve can lead to several disease states. One is mixed secretory-osmotic diarrhea. Decreased ileal reabsorption of bile salts results in fat malabsorption and steatorrhea. The presentation of increased amounts of bile salts and fatty acids to the colon decreases water absorption and stimulates active chloride and water secretion, producing a cholera-like high-volume secretory diarrhea. The loss of the ileocecal valve and ileum segment accelerates intestinal transit time, which does not allow for complete digestion and absorption of food. Water and electrolytes remain associated with undigested food particles and may overwhelm the absorptive capacity of the colon, resulting in an osmotic diarrhea. A second problem is vitamin B12 deficiency. Surgical reduction of sites in the terminal ileum for active and exclusive uptake of vitamin B12 might lead to hypovitaminosis. If this is unrecognized, patients may develop irreversible neurologic injury. A third problem is cholelithiasis. Derangements in bile salt metabolism can occur when as little as 10 cm of ileum is resected, and the propensity to form gallstones is increased. Pigment gallstones appear to be the predominant stone associated with ileal resections. The fourth possible problem is urolithiasis, the etiology of which is multifactorial in patients with ileal resections. With decreased availability of bile salts, fat malabsorption occurs. Fatty acids bind with calcium and magnesium to form soaps, resulting in increased levels of free oxalate available for absorption. Moreover, fatty acids directly increase colonic permeability to oxalate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutritional and gastrointestinal complications of the use of bowel segments in the lower urinary tract. 194 6

There are differences between young and adult organisms regarding toxokinetic aspects and clinical manifestations of heavy metal intoxications. Chronically, toxic Cd intake causes a microcytotic hypochromic anemia in young rats at lower exposure levels and after shorter exposure periods than in adult animals. Cd absorption is increased by co-administration of milk and in conjunction with iron deficiency. After long exposure periods toxic Cd concentrations accumulate in the kidney cortex; this process starts very early in life. In 3-year-old children Cd concentrations in the kidney can reach up to one-third of those found in adults. Hg++ and methyl-Hg can cause Hg encephalopathia, and frequently cause mental retardation in adults. Correspondingly, Hg++ accumulation in the brains of suckling rats is approx. 10 times higher than in grown animals. Milk increases the bioavailability of Hg++. In suckling rats Hg is bound to a greater extent to ligands in the erythrocytes. Methyl-Hg concentrations in breast milk reach 5% of those in maternal plasma and that is a severe hazard for breastfed children of exposed mothers. Toxic Pb concentrations can lead to Pb encephalopathia. A high percentage of surviving children have seizures and show signs of mental retardation. Anemia and reduced intelligence scores were recently observed in children after exposure to very low levels of Pb. Pb absorption is increased in children and after co-administration of milk. There are no definite proofs for carcinogenesis or mutagenesis after oral exposure to Cd, Hg, and Pb in man. Heavy metal concentrations were found in the same order of magnitude in commercial infant formulas and in breast milk. When infant formulas are reconstituted with contaminated tap water, however, Pb and Cd concentrations can be much higher. The average heavy metal uptake from such diets exceeds the provisional tolerable weekly intake levels set by the WHO for adults, calculated on the basis of an average food intake and a downscaled body weight. These considerations do not even provide for differences in absorption and distribution or for the increased sensitivity of children to heavy metal exposure. However, dilution effects for essential heavy metals were observed in fast-growing young children; this effect might be extrapolated to toxic metals. These theoretical considerations are compared with epidemiological evidence. A health statistic from Baltimore shows a decline of Pb intoxications in infants. This observation correlates with a simultaneous decline in exposure to Pb which was due, for example, to decreased use of lead dyes in house paints and the abolition of tin cans for infant food.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The toxicological estimation of the heavy metal content (Cd, Hg, Pb) in food for infants and small children]. 218


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