Absorption Of 59Fe Research Articles

Altered absorption and regulation of iron in chicks with acute Salmonella gallinarum infection

Chicks aged 15 days were infected orally with Salmonella gallinarum. During the six-day period immediately following infection the absorption of 59Fe from the gut fell progressively to be eventually about half that in noninfected chicks. This reduced uptake was accompanied by a shift in the distribution of the 59Fe absorbed, more occurring in the spleen and less in the liver and blood. During the eight-day period that immediately followed infection in another experiment, serum iron concentration on day 4 and 6 in infected chicks was significantly lower than that in noninfected birds. In the infected chicks also the transferrin saturation was significantly lower and the unsaturated ironbinding capacity higher, on days 4, 6, and 8 after infection. These findings show that there is a major disturbance in iron regulation in acute systemic bacterial infection in the immature fowl and suggest that the mild anaemia which occurs in chicks during acute S gallinarum infection a shortage of iron in the body.

Measurement of 59Fe absorption and retention in patients with familial chronic muco-cutaneous candidiasis using the method of whole body counting.

A study of 59Fe absorption was carried out on fourteen patients with familial chronic muco-cutaneous candidiasis (FCMC) using the method of whole body counting. 59Fe retention was also determined in eleven of these individuals, for periods up to 133 days. Eight of fourteen patients absorbed less than 6% of the 59Fe administered. Six of these subjects had previously shown evidence of impaired iron tolerance in the presence of latent iron deficiency. Iron excretion was not increased in any of the individuals studied. These observations support the view that iron absorption may be impaired in some patients with FCMC and could be a contributory factor in the aetiology of the latent iron deficiency associated with the condition.

Iron Availability to Rats from Soybeans

Experiments were carried out to determine the effects of endogenous phytic acid in soybean seeds (Glycine max, var. "Amsoy") on the bioavailability of 59Fe to iron-depleted rats. Soybean plants were grown in nutrient solutions labeled with 59Fe supplied at either 0.4 or 1.0 ppm iron in solution. Immature and mature soybean seeds were harvested and fed to male rats as a single dose. The phytic acid content of the immature and mature seeds averaged 0.61 and 1.71% dry weight, respectively. Varying the nutrient solution iron concentration in the mature soybean seeds. When the 59Fe-labeled seeds were fed to iron-deficient rats, 59Fe from the mature seeds was more available than that from immature seeds even though the mature seeds contained approximately three times as much phytic acid. Autoclaving the mature seeds did not affect the absorption of 59Fe by rats from the seeds. Immature soybean seeds contained much more insoluble 59Fe than did mature soybean seeds. It was concluded that the directly correlated to the phytate content of the seeds; also immature soybean seeds apparently contain a factor or factors (other than phytic acid) that depresses iron availability.

Intestinal iron absorption under the influence of available storage iron and erythroblastic hyperplasia

A high negative correlation (coefficient similar to 0.9) between increased 59Fe absorption from a diagnostic 0.56 mg 59Fe2+ dose and the depletion of available storage iron was observed in menstruating and pregnant women, fullterm and premature infants, blood donors, patients with infections, inflammations, tumors, hepatic cirrhosis, gastric surgery, increased urogenital or gastrointestinal blood loss. The increased diagnostic 59Fe2+ absorption is a reliable and sensitive indicator of at least depleted iron stores or prelatent iron deficiency as caused by iron malnutrition or maldigestion, increased iron requirement in pregnancy, infancy, urogenital or gastrointestinal blood loss. Although the messenger system which signalyzes the depletion of iron stores to the iron absorbing enterocytes of the duodenal and jejunal mucosa is not yet known available storage iron seems to control intestinal iron absorption under normal and the great majority o pathological condition in humans. Anemia per se or high erythropoietin levels in blood do not influence iron absorption since patients with even severe erythroblastic hypoplasia, aplastic anemia and megaloblastic anemia due to vitamin B12 deficiency absorb iron according to their iron stores. An only mild hyperplasia of the erythropoietic system in the bone marrow does also not effect iron absorption which was still under the control of available storage iron in patients with hereditary spherocytosis, nonspherocytic congenital hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency, acquired hemolytic anemia and vitamin B12 deficiency induced megaloblastic anemia..

Absorption of inorganic and food iron in children with heterozygous and homozygous beta-thalassemia.

The intestinal absorption of 59Fe from a diagnostic 10 μmole (0.56 mg) 59Fe2+ test dose and 5 mg Fe equivalents of 59Fe-labeled pork, hog liver and hemoglobin was measured with a 4 π geometry whole-body radioactivity detector with liquid organic scintillator and the results compared with the stainable amounts of diffuse cytoplasmatic (non-heme) storage iron in the bone marrow macrophages, serum iron concentrations and total iron-binding capacity, erythropoietic activity and other hematological parameters. Children with mild hypochromic, microcytic anemia due to heterozygous β-thalassemia absorbed normal amounts of 59Fe from the diagnostic dose of 59Fe2+ if their bone marrow macrophages contained normal or mildly increased amounts of diffuse cytoplasmatic storage iron. Depleted iron stores also caused increased absorption of diagnostic 59Fe in children with heterozygous β-thalassemia, so that prelatent iron deficiency can be diagnosed by measurement of increased iron absorption.

The subcellular distribution of 59 Fe in small intestinal mucosa: studies with normal, iron deficient and iron overloaded rats.

SummaryIron deficient and iron loaded rats were given 59Fe by stomach tube and the subcellular distribution of 59Fe in the intestinal mucosa was investigated. There was considerable concentration of 59Fe in the soluble fraction shortly after administration of the dose but concentration in the mitochondria at 12 and 18 hr. Concentration in the mitochondria was particularly marked in the iron deficient rats. After intravenous injection of 59Fe normal, iron deficient and iron loaded rats all showed the greatest concentration of the isotope in the mitochondrial fraction. The incorporation of 59Fe into ferritin was not greater in the iron loaded rats than in normal rats, although the absorption of 59Fe was only one third of the normal level. In iron deficiency very little radioiron was incorporated into ferritin. These results support the suggestion that ferritin formation may not be a major controlling factor in iron absorption and demonstrate the need to consider the role of mitochondria in iron transport within the intestinal epithelial cell.

Effect of Histidine and Ascorbic Acid on the Absorption and Retention of 59Fe by Iron-depleted Rats

Effect of Histidine and Ascorbic Acid on the Absorption and Retention of 59Fe by Iron-depleted Rats

59Fe 2+- and hemoglobin- 59Fe absorption in human beings do not require gastric juice or intrinsic factor

The intestinal 59Fe absorption from 10-μmole (=0.56 mg) 59Fe 2+ and hemoglobin- 59Fe as well as from 5.0-mg hemoglobin- 59Fe doses was measured with the 59Fe-absorption whole-body retention test in normal volunteers and in vitamin-B 12-treated pernicious anemia patients with gastric atrophy and absolute intrinsic-factor deficiency. A completely normal 59Fe absorption from ferrous iron and hemoglobin iron at the 0.56-mg iron level was observed in all the patients without gastric juice. At the 5.0-mg iron dose level hemoglobin- 59Fe was even better (2-fold) absorbed in patients with absolute intrinsic-factor deficiency and a purified hog intrinsic-factor concentrate of known potency did not influence the already doubled hemoglobin- 59Fe absorption. Depleted iron stores in prelatent iron deficiency resulted in a 4-fold increase of 59Fe 2+ absorption and a 50% increase of hemoglobin- 59Fe absorption also in patients without gastric juice and without intrinsic factor. Gastric juice or a gastric intrinsic factor are therefore not required for intestinal ferrous iron or hemoglobin-iron absorption in humans.

Absorption of 59Fe in the rat: Iron binding substances in the soluble fraction of intestinal mucosa

The soluble fraction of homogenised intestinal epithelial cells has been obtained from rats killed during the process of radioiron absorption. Starch gel electrophoresis shows the presence of four distinct iron binding proteins. Protein I is ferritin. Protein II appears to be transferrin. Protein IV is a high molecular weight mucoprotein which appears to be closely related to the absorption process.

Comparative absorption of ferri-haemoglobin- 59 Fe-Ferro-haemoglobin- 59 Fe and 59 Fe 3+ - 59 Fe 2+ in humans with normal and depleted iron sotres.

Abstract. The intestinal 59Fe absorption from ferri‐ and ferro‐haemogIobin‐59Fe and 59Fe3+ and 59Fe+ was calculated from whole body‐59Fe‐retention measurements in subjects with normal and depleted iron stores. A ferri‐haemoglobin‐59Fe/ferro‐haemoglobin‐59Fe absorption ratio of 1.03 ±0.11 was observed for the absorption of ferri‐haemoglobin‐59Fe (8.6± 0.77%) and ferro‐haemogIobin‐59Fe (8.7±0.94%) in persons with normal iron stores. Depletion of iron stores caused a slight but significant higher rise of ferri‐haemoglobin‐59Fe absorption (22 ± 1.7%) than the increase of ferro‐haemoglobin‐59Fe absorption (18 ±0.9%) so that the absorption ratio was 1.24±0.073.—This remarkable iron valence independence of haemoglobin iron absorption is in considerable contrast to the well‐established valence dependence of inorganic iron absorption which favours ferrous iron absorption especially with rising iron doses. The 59Fe3+/59Fe2+ absorption ratio for a diagnostic 0.56 mg Fe dose increased from 0.43 in subjects with normal iron stores to 0.74 in persons with depleted iron stores, whereas this absorption ratio was augmented only from 0.21 to 0.28 for the therapeutic 50 mg Fe‐dose.—The different influence of iron valence on iron absorption from inorganic and haemoglobin iron supports other evidence for the existence of two separate mechanisms for ferrous iron and haem iron absorption in humans.

Effect of anticholinergic agents on the intestinal absorption of 59 Fe ferrous citrate.

The absorption of59Fe ferrous citrate has been studied in humans after administration of the anticholinergic agent, hexocyclium methosulfate, and in rats, after atropine. In both species, anticholinergics produced a decrease in absorption. The effect of atropine on iron absorption persisted when the radioiron was delivered intragastrically, mixed with gastric juice, but not when administered intraduodenally. Another set of experiments showed that iron absorption decreases when radioiron is intraduodenally delivered in deproteinized acid gastric juice, or in 0.10 N HCl, but not when mixed with neutralized gastric juice. It is concluded that anticholinergic drugs inhibit iron absorption by an effect on a gastric factor necessary for optimal iron absorption, and not through a decrease in acid secretion.

Experimental achylia gastrica and iron absorption.

Summary. Achylia gastrica with lowered iron stores was produced in rats by direct X‐irradiation of the exposed stomach. Absorption of 59Fe as a ferrous salt was measured in these and in normal and iron‐deficient control rats to study the effect of various components of gastric juice on iron absorption. Hydrochloric acid had no effect in rats with achylia gastrica, but neutralized rat gastric juice, pernicious anaemia gastric juice, and intrinsic factor increased absorption two‐fold. Untreated rat and human gastric juice increased absorption four‐fold while antigastric mucosal serum reduced absorption four‐fold. This reduction was corrected by adding rat gastric juice. Gastric juice appears to play a significant role in iron absorption.

IRON ABSORPTION FROM BROWN BREAD

Four volunteers each used a brown loaf labelled with 59Fe as her sole source of bread for 3-5 days. 59Fe absorption was measured with a total body counter. The results suggest that brown bread may be a better source of dietary iron than white bread enriched with iron.

Effect of Histidine and Certain Other Amino Acids on the Absorption of Iron-59 by Rats

Reports in the literature have indicated that several amino acids can increase the absorption of ferrous iron. The objectives of the experiments reported here were to determine if certain amino acids would increase absorption of 59Fe supplied in the ferric form and, if so, to investigate the mechanism of action of these amino acids. Of six amino acids tested, histidine and lysine significantly increased 59Fe absorption from ligated, in vivo, duodenal segments, whereas glutamine, glutamic acid, methionine, and glycine did not. Further, histidine was not effective if administered intraperitoneally or if put into an intestinal segment adjacent to the one in which 59Fe was administered. When histidine was added to an 59Fe solution which contained ascorbic acid, it increased absorption over and above that observed with ascorbic acid alone. In all of these studies, histidine increased 59Fe uptake only if histidine and 59Fe were administered in the same solution. This suggests some direct reaction between iron and histidine and is consistent with the hypothesis that an amino acid-iron chelate is formed and subsequently absorbed. Since histidine is a product of protein hydrolysis in the gastrointestinal tract, it may be involved in the normal absorption of iron.

Studies of Iron Transport in Portal and Systemic Circulation

Abstract Simultaneous 59Fe absorption curves in portal and systemic venous blood showed different rates of entry of the isotope into the portal (and systemic) circulation: the most rapid entry was seen in two patients with decreased iron stores, whereas negligible counts were obtained in two patients with increased iron stores. These data, combined with 59Fe excretion data, indicate a barrier function of the intestinal mucosa for the passage of iron in two iron-sufficient patients, with evidence of prolonged excretion of 59Fe into the bowel in one of these. The data support a two-step mechanism of absorption of inorganic ferrous iron in humans, the first step being uptake of iron by the intestinal mucosa; the second step transfer of mucosal iron to the portal circulation. In the two patients with decreased iron stores the shape of the absorption curves ruled out significant hepatic deposition of isotope; the amount of isotope transported in the systemic circulation correlated closely with that utilized for hemoglobin synthesis. Different rates of absorption of inorganic ferrous iron and folic acid were demonstrated in one patient.

Comparative physiological study of iron, manganese and copper absorption by plants

Abstract In the previous reports, influence of metabolic inhibitors, such as NaCN, 2,4-dinitrophenol and EDTA, on the absorption of 59Fe, 54Mn and 64Cu(1) and the distribution of these elements in root cell were studied using the separation technique by centrifugal forces (2). These experiments revealed that rice and barley plants behave differently in their mode of absorption and distribution of these elements.

Influence of Various Chelating Agents on Absorption of 60Co, 59Fe, 54Mn and 65Zn by Chickens

KRATZER et al. (1959) observed that turkey poults, fed an isolated soybean protein diet, recovered from the zinc deficiency when small amounts of EDTA (ethylenediaminetetraacetic acid) were fed in the ration. Similar effects of EDTA have been reported for chickens (O’Dell et al., 1964) and for rats (Oberleas et al., 1966). EDTA was reported to decrease iron availability to rats (Larsen et al., 1960) and to reduce cobalt toxicity in chickens (Turk and Kratzer, 1960). The nature of this chelation was studied by Vohra and Kratzer (1964) and by Nielsen et al. (1966) using different chelating agents. They found that the availability of zinc was increased as the stability constants of the chelating agents increased. The greatest response to the chelating agents was obtained when sequestrenes having stability constants between 14 and 15 were fed. Growth rate and the healing of zinc deficiency symptoms decreased as the stability constant values .

USE OF RADIOACTIVE 59Fe FOR TRACING SOIL PARTICLE MOVEMENT

SummaryThe field studies reported in Part 1 were complemented by laboratory investigations on the labelling of soils and the movement of soil particles by simulated rainfall splash.Of various labelling techniques tested the most uniform absorption of 59Fe, as shown by autoradiographs, was secured by adding DTPA chelating reagent to the FeCl3 solution used for wetting soil peds under vacuum. Studies on the specific radioactivity of the Atterberg textural fractions, separated from clayloam, sandy loam, loam and peat soils before and after labelling, showed in all cases that the clay fraction was dominant in retention of 59Fe.The radioactivity was so firmly absorbed that its movement could be used to trace both the horizontal and vertical displacements of labelled soil particles by scintillation counting or autoradiographic techniques. Tests with a rainfall simulator showed a close correlation between the weights and radioactivities of splashed soil particles.Gravimetric data obtained from unlabelled clay loam and sandy loam soils subjected to ‘rainfall’ of differing intensity, drop size and height of fall gave a linear relationship on a logarithmic scale between mass of particles and distance of splash. Calculation of the kinetic energy lost by water drops on impact with the soil and that imparted to the splashed soil particles show that the relationship depends principally on the rainfall intensity and the texture of the soil.

59Fe Absorption by Chickens

No quantitative information is available on the absorption of iron by chickens. Elvehjem and Hart (1929) demonstrated that an anemia of chickens fed a milk diet could be corrected by iron and copper supplementation. Hill and Matrone (1961) reported extensive studies on the metabolism and requirements of growing chickens for iron and copper and concluded from their results that 4 p.p.m. of copper and 40 p.p.m. of iron were needed in the diet to satisfy the chickens’ requirements for these elements.This study was initiated to determine to what extent an oral 59Fe dose could be absorbed by chickens receiving diets deficient or adequate in iron and copper.EXPERIMENTALEighty, day-old New Hampshire female chickens were fed the skim milk diet described by Hill and Matrone (1961) supplemented with 100 p.p.m. of Fe and 10 p.p.m. Cu for two weeks. They were then divided into two groups: one was fed .

Effects of Dietary Iron Level on Gut Iron Levels and Iron Absorption in the Rat

The proposal that the iron content of the intestine is of critical importance in determining the rate of iron absorption was examined in Sprague-Dawley rats. The iron content of the rat gut was found to vary with the iron content of the diet but the relationship was not a linear one. The more proximal sections of the gut were more sensitive to dietary iron level than the distal portions. Rats fed stock ration had much lower proximal gut iron levels than rats fed purified diets of lower iron content. The iron content of the gut appeared to influence, within limits, the absorption of 59Fe from an isolated gut loop. When rats were transferred from a high iron diet to a low iron diet, a steady depletion of iron from the gut was accompanied by an increase of iron absorption which was maximum on the third to fifth day after the change of diet. In the reverse experiment, iron absorption was almost immediately depressed concomitant with the elevation of the gut iron level. The iron content of the mucosa did not appear to influence the entrance of the test dose of iron into the mucosa. Rather, the major point of mucosal regulation appeared to be the transfer of iron from the mucosa to the blood supply. The failure of a large dose of iron placed in the jejunum to influence immediately the absorption of 59Fe from a duodenal loop indicates that extra-mucosal (hormonal?) control of iron absorption is minimal or lacking.