Body Iron Content Research Articles

Effects of dietary ascorbic acid/iron ratio on some production traits, lipid peroxide state and amount/activity of the glutathione redox system in African catfish Clarias gariepinus (Burchell) fingerlings

African catfish Clarias gariepinus (Burchell) fingerlings (3.16–3.92 g initial body weight) were investigated for 30 days in four different groups using different amounts of l-ascorbic acid (AA) and iron (supplied as FeC6H5O7) in their feedings. Diet 1 (control): no addition of AA or iron; diet 2 (H-AA/FE): high (600 mg kg−1) AA and low (218 mg kg−1) iron; diet 3 (H-HE/AA): high (364 mg kg−1) iron and low (200 mg kg−1) AA; and an unfed group, which was investigated only for 15 days due to high mortality. The live weight gain, feed intake, specific growth rate (SGR; % body weight day−1) and feed conversion rate (FCR) were measured or calculated. At the end of the experimental period, the whole body content of AA, iron, reduced glutathione (GSH), glutathione disulphide (GSSG) and malondialdehyde (MDA), as well as the glutathione peroxidase (GSHPx) activity, were measured. The production traits did not differ significantly as a result of the different AA and iron contents of the feed. AA content increased significantly in all the groups as compared with the initial value, except in the unfed group. The difference between the treated groups as compared with the control, with regard to the two AA/iron treated groups, was also significant. The iron content in the fish body increased significantly compared with the initial value, except in the unfed group. The difference compared with the control was significant only in the H-FE/AA group. The difference between the groups that consumed low and high iron content diets was also significant. The GSH and GSSG content, as well as the GSH/GSSG ratio and GSHPx activity of the fish body, did not differ significantly as compared with the initial value or with the control. The lipid peroxide status, as measured by the MDA content, did not differ significantly either as an effect of the AA and iron supplementation, but decreased as an effect of ageing and starvation. It may be concluded that, under the present experimental conditions, the C. gariepinus fingerling tissue stores of AA and/or iron increased as a result of feed supplementation, but without altering the actual lipid peroxide status and the amount/activity of the glutathione redox system.

Iron balance and iron nutrition in infancy.

At birth, the total body iron content is approximately 75 mg/kg, twice that of an adult man in relation to weight. During the first 6 mo of life, total iron body content increases slightly and exclusive breastfeeding is sufficient to maintain an optimal iron balance. Thereafter, iron body content substantially increases and the infant becomes critically dependent on dietary iron, provided by complementary foods. Numerous factors may contribute to nutritional iron deficiency in infancy, the most important being low body iron content at birth, blood loss, high postnatal growth rate, and a low amount and/or bioavailability of dietary iron. We have documented that the prevalence of iron deficiency declined in Italy as iron nutrition improved and that early feeding on fresh cow's milk is the single most important determinant of iron deficiency in infancy. Healthy full-term infants should maintain optimal iron balance by consuming a good diet, which can be summarized as follows: breastfeeding should be continued exclusively for at least 5 mo and then together with complementary foods containing highly bioavailable iron; infants who are not breastfed or are partially breastfed should receive an iron-fortified formula, containing between 4.0 and 8.0 mg/L iron, from birth to 12 mo of age; fresh cow's milk should be avoided before 12 mo of age.

Iron balance and iron nutrition in infancy

At birth, the total body iron content is approximately 75 mg/kg, twice that of an adult man in relation to weight. During the first 6 mo of life, total iron body content increases slightly and exclusive breastfeeding is sufficient to maintain an optimal iron balance. Thereafter, iron body content substantially increases and the infant becomes critically dependent on dietary iron, provided by complementary foods. Numerous factors may contribute to nutritional iron deficiency in infancy, the most important being low body iron content at birth, blood loss, high postnatal growth rate, and a low amount and/or bioavailability of dietary iron. We have documented that the prevalence of iron deficiency declined in Italy as iron nutrition improved and that early feeding on fresh cow's milk is the single most important determinant of iron deficiency in infancy. Healthy full-term infants should maintain optimal iron balance by consuming a good diet, which can be summarized as follows: breastfeeding should be continued exclusively for at least 5 mo and then together with complementary foods containing highly bioavailable iron; infants who are not breastfed or are partially breastfed should receive an iron-fortified formula, containing between 4.0 and 8.0mg/L iron, from birth to 12 mo of age; fresh cow's milk should be avoided before 12 mo of age.

Respiratory function in patients with thalassaemia major: relation with iron overload

Aims: (1) To determine the pattern of respiratory impairment in children with thalassaemia major (TM); (2) to assess the relation between the degree of respiratory impairment and total body iron...

Uterine peristaltic activity during the menstrual cycle: characterization, regulation, function and dysfunction

AbstractUnlike other smooth muscle organs, the uterine muscle was regarded to be normally functional for only a brief period, following a lengthy gestation. However, recently it has been shown that uterine peristalsis constitutes one of the fundamental functions of the non-pregnant uterus. Its morphological basis is the archimyometrium, which is the muscular component of the archimetra and which preserves a functional bipartition of the primarily unpaired uterus. Three types of uterine peristaltic contractions can be distinguished: cervico–fundal, fundo–cervical and isthmical peristaltic activity, which changes during the menstrual cycle and is controlled by the dominant ovarian structure via the secretion of sex steroids systemically and into the utero-ovarian vascular countercurrent system. Uterine peristalsis of the non-pregnant uterus is actively involved in very early reproductive processes, such as rapid and sustained directed sperm transport and high fundal implantation, as well as serving retrograde menstruation for the preservation of body iron content. Furthermore, it became apparent that hyper-and dysfunctions of this contractile activity, such as hyper- and dysperistalsis, might be causally involved in the development of pelvic endometriosis, uterine adenomyosis and infertility, as obtained from immunohistochemistry, vaginal sonography, hysterosalpingoscintigraphy and magnetic resonance imaging.

Neonatal iron nutrition

Preterm infants are prone to iron deficiency. Their total body iron content at birth is low and gets further depleted by clinical practices such as uncompensated phlebotomy losses and exogenous erythropoietin administration during the neonatal period. Early iron deficiency appears to adversely affect cognitive development in human infants. To maintain iron sufficiency and meet the iron demands of catch-up postnatal growth, iron supplementation is prudent in preterm infants. A dose of 2–4mg/kg/day is recommended for preterm infants who are fed exclusively human milk. A dose of 6mg/kg/day or more is needed with the use of exogenous erythropoietin or to correct preexisting iron deficiency. However, due to the poor antioxidant capabilities of preterm infants and the potential role of iron in several oxidant-related perinatal disorders, indiscriminate iron supplementation should be avoided.

Of metals, mice, and men: what animal models can teach us about body iron loading.

Of metals, mice, and men: what animal models can teach us about body iron loading.

Spray‐Dried Blood Cells as a Partial Replacement for Fishmeal in Diets for Rainbow Trout Oncorhynchus mykiss

Abstract.— The objective of this study was to evaluate growth of juvenile rainbow trout Oncorhynchus mykiss (81.4 mm initial length and 6.4 g initial weight) fed a diet containing 47.5% herring meal (FM diet) and a test diet containing 34.5% herring meal and 8.75% spray‐dried animal blood cells (SBC diet). Both diets were formulated to be isonitrogenous (48.5 and 48.0% protein) and isocaloric (3,977 and 3,927 kcal DElkg). At the end of the 12‐wk feeding trial, differences in growth rate and feed conversion ratios were not statistically significant between the two dietary treatments. Apparent crude protein digestibility was 89.7% for the SBC diet and 88.1% for the FM diet. Apparent net protein utilization and iron retention values were not different, but phosphorus retention was higher for fish fed the SBC diet. Whole body iron content of the fish decreased in both groups from 23.3 mg/ kg in an initial sample to 16.5 mg/kg in fish fed the FM diet and 18.4 mg/kg in fish fed the SBC diet at the end of 12 wk. The diet containing 8.75% SBC replaced 27.4% of the crude protein supplied by herring meal, and it had 22.7% less total phosphorus (P) than the fishmeal diet. The cost of gain for the FM diet was $0.508/kg gain compared to $0.512/kg gain for the SBC diet.

Kupffer cell staining by an HFE-specific monoclonal antibody: implications for hereditary haemochromatosis.

Hereditary haemochromatosis is an inherited disorder of iron absorption that leads to excessive iron storage in the liver and other organs. A candidate disease gene HFE has been identified that encodes a novel MHC class I like protein. We report the development of a monoclonal antibody (HFE-JB1) specific for recombinant refolded HFE protein. The antibody immunoprecipitates a 49 kD protein from the cell line U937, a histiocytic lymphoma. It binds HFE but does not recognize other recombinant non-classic MHC class I proteins (HLA-E, F and G), nor does it react with a variety of recombinant classic class I MHC molecules. COS cells transfected with HFE in culture are stained specifically. The immunohistochemical staining pattern in human tissues is unique and can be defined as a subset of the transferrin receptor positive cells. In the liver HFE protein was shown to be present on Kupffer cells and endothelium (sinusoidal lining cells), but absent from the parenchyma. Kupffer cells from an untreated C282Y HH patient failed to stain with the antibody. In the normal gut scattered cells in the crypts are stained. HFE was also present on capillary endothelium in the brain (a site of high levels of transferrin receptor) and on scattered cells in the cerebellum and cortex. These results raise interesting questions concerning the function of HFE in the control of body iron content and distribution.

Assessment of hepatic iron overload in thalassemic patients by magnetic resonance spectroscopy

The transverse relaxation time of water protons is shortened by the presence of iron. This shortening depends on the amount and the environment of iron in the sample. We have developed a method for measuring short transverse relaxation time noninvasively by magnetic resonance spectroscopy. To evaluate magnetic resonance spectroscopy as a means of assessing hepatic iron content in patients with transfusional iron overload, we compared the results obtained with this method with those obtained by other means of assessing total body iron content. The correlation between the liver biopsy iron concentration and 1/transverse relaxation time was highly significant (r = 0.95, p < 0.004, n = 6) for iron loads up to 3% dry weight. The correlation between serum ferritin and 1/transverse relaxation time was also significant, but the correlation coefficient was much lower (r = 0.67, p < 0.002, n = 20). The correlation between 24-hr urinary iron excretion and 1/transverse relaxation time was not significant, nor was that between AST and 1/transverse relaxation time. We conclude that magnetic resonance spectroscopic determination of the transverse relaxation time of hepatic water is an accurate method of measuring liver iron content, especially when the iron content is below 3%. Because it is a noninvasive method that is associated with negligible side effects, it could provide clinicians with an excellent means of assessing the effectiveness of the various therapeutic strategies used in the management of patients with iron overload.

Assessment of hepatic iron overload in thalassemic patients by magnetic resonance spectroscopy

The transverse relaxation time of water protons is shortened by the presence of iron. This shortening depends on the amount and the environment of iron in the sample. We have developed a method for measuring short transverse relaxation time noninvasively by magnetic resonance spectroscopy. To evaluate magnetic resonance spectroscopy as a means of assessing hepatic iron content in patients with transfusional iron overload, we compared the results obtained with this method with those obtained by other means of assessing total body iron content. The correlation between the liver biopsy iron concentration and 1/transverse relaxation time was highly significant (r = 0.95, p < 0.004, n = 6) for iron loads up to 3% dry weight. The correlation between serum ferritin and 1/transverse relaxation time was also significant, but the correlation coefficient was much lower (r = 0.67, p < 0.002, n = 20). The correlation between 24-hr urinary iron excretion and 1/transverse relaxation time was not significant, nor was that between AST and 1/transverse relaxation time. We conclude that magnetic resonance spectroscopic determination of the transverse relaxation time of hepatic water is an accurate method of measuring liver iron content, especially when the iron content is below 3%. Because it is a noninvasive method that is associated with negligible side effects, it could provide clinicians with an excellent means of assessing the effectiveness of the various therapeutic strategies used in the management of patients with iron overload.

Inhibition of iron absorption prolongs the life span of Drosophila

The life span of Drosophila melanogaster (Oregon R) males was found to be proportional to the logarithm of the iron content of the diet. Life span was also shown to be proportional to the rate of iron accumulation for Drosophila, mice and man. The total body iron content was found to correlate with the total calcium content of adult Drosophila. Iron content during the developmental stages, however, remained relatively constant and did not change with changes in the calcium concentrations. Dietary tea ( Camellia sinensis) extracts were found to inhibit the ageing-related accumulation of iron and to prolong the life span of Drosophila by as much as 21.4%. It is concluded that iron accumulation is a significant factor contributing to senescence.

Endogenous iron excretion

The effects of supplemental oral (0, 40, and 400 ppm) and parenteral iron (0 and 2.72 mg Fe iv given initially as a single dose) on iron absorption, excretion, and retention were determined in 30 rats. Endogenous fecal iron excretion was determined by the radioisotope dilution technique after im injection of 80 kBq Fe-59, using blood and certain body tissues as reference sources for the estimation of the specific activity (Bq Fe-59/micrograms Fe) of endogenous iron. The basal diet contained 3.6 ppm Fe. Fe(III)-hydroxide-polymaltose was used as the sole iron source in oral, iv, and im iron treatments. Iron balance as determined from day 14 to 20 of the experiment was not significantly affected by iv iron administration. Nevertheless, a temporarily reduced retention should have occurred, since differences in final body iron contents were lower than 2.72 mg, as compared to the respective untreated groups. Apparent iron absorption and iron retention increased with surplus oral iron, and the efficiency rates were highest with adequate iron supply (40 ppm). True absorption rates of iron were similar without any, and with 40 ppm Fe amounting 40 to 50% of the intake. In the iron deficient rats, half of the actually absorbed iron (about 16 micrograms/d) was lost by endogenous fecal re-excretion, and another 3 micrograms/d by the urinary route. Endogenous loss with feces and with urine increased with further oral iron supply, but at a considerably lower rate as total fecal excretion. Parenterally administered iron did not affect endogenous loss at all. The results indicate that endogenous excretion cannot be regarded as a means to eliminate excessive iron, and might actually be an inevitable loss.

Small‐dose iron tolerance test and body iron content in normal subjects

The small-dose iron tolerance test (SD-ITT) was performed in 37 healthy subjects (20 females and 17 males). The area under the curve (AUC) of serum iron variations after the test dose (10 mg of iron as iron sulphate) was corrected by the expected plasma iron disappearance rate, the expected subject's plasma volume and the measured spontaneous time-dependent serum iron variations, and was used as a summary measure of the outcome, Q-ITT. Q-ITT correlated strictly with the maximum serum iron increase (SImax). Q-ITT gave positive (greater than zero) values in only 14 out of the 37 subjects (11 females and 3 males). Serum ferritin proved to be the best discriminating parameter between positive and non-positive subjects, and was inversely correlated with Q-ITT in the positive ones. In 2 male subjects, aged 43 and 34 years, SD-ITT proved to be highly sensitive to the progressive decrease of mobilizable body iron content during repeated venesections. In these patients the threshold for a positive test result was obtained at values lower than 1050 and 950 mg of body iron content, respectively. The threshold-dependent sensitivity, simplicity, and repeatability of this method favor its becoming a useful technique for studying the up-regulation of iron absorption in normal subjects and in pathological conditions.

Body and egg iron content in shaver and new hampshire chickens

1. 1. A comparative study on the iron content in internal organs (blood, liver, spleen, kidneys and heart), carcass and feathers, as well as on the whole iron content has been carried out at different ages (4, 8, 13, 18 and 24 weeks), on two chicken breeds (shaver and New Hampshire). 2. 2. The iron content in internal organs in shaver was higher than in New Hampshire. 3. 3. A tendency of the iron content in the carcass to decrease with age has been observed for both breeds; values were higher for laying shaver hens. 4. 4. The egg-producing strain, shaver, showed a greater iron status with a stable body iron content from 13 weeks on (53–55 ppm), permitting a constant laying frequency (90%) during an 18-month period, with only a small reduction of egg iron content from 33.8 to 31 ppm. 5. 5. The whole body iron decreased progressively with age in the New Hampshire broiler strain to 42–49 ppm iron, and the laying process sharpened this tendency. A drastic reduction in laying, accompanied by a lower egg iron content (28.9 ppm iron), was observed. 6. 6. Iron data obtained in the present paper reflect the specific genetic adaptation to egg production of the shaver strain.

Age-related changes in the kinetics of iron absorption across the guinea pig proximal intestine in vivo.

In the healthy human adult, body iron content is regulated by intestinal iron absorption. However in neonates who are iron replete, iron absorption is inappropriately increased. In this study we have compared the kinetics of iron absorption in the proximal small intestine of the newborn and adult guinea pig in order to gain insight into the cellular mechanisms underlying this difference. Iron uptake was studied in vivo over the concentration range 20-2,000 microM. Total iron uptake could be resolved into saturable and linear components. The kinetic constants for the saturable component in the adult were similar to the neonate. In contrast, the rate of uptake via the linear pathway was 4 times greater in the neonate compared to the adult. It is concluded that the increased absorption of iron by the neonatal guinea pig is due to an enhanced uptake via the linear pathway. In contrast to total iron uptake, we were unable to detect developmental changes in iron transfer into the carcass.

From the NIH

Patients with disorders such as Cooley's anemia (severe β-thalassemia) or hereditary hemochromatosis have elevated levels of total body iron that must be treated. John Harris, MD, and Gary Brittenham, MD, at Case Western Reserve University School of Medicine, Cleveland, have developed a magnetic device that can noninvasively determine body iron content. The instrument, known as a superconducting quantuminterference device (SQUID) susceptometer, will allow earlier identification than is now possible of patients at risk of iron overload. This device is believed to be the only instrument of its kind in the world at present. Its developers have received grant support from the National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, Bethesda, Md, a part of the National Institutes of Health. The normal adult body contains about 4 g of iron, of which 3 g are involved in oxygen transport and storage. Approximately 1 g is in two specialized proteins,

Idiopathic hemochromatosis: serum ferritin concentrations during therapy by phlebotomy.

We report the case of a 54-year-old man who presented with symptoms of idiopathic hemochromatosis, an inherited disorder involving regulation of iron absorption. These symptoms usually do not appear until total body iron content reaches 15 g, about threefold normal. Therapy involves mobilization and removal of excess stored iron through weekly or twice-weekly phlebotomies of 500 mL, until the hemoglobin concentration becomes less than 110 g/L and remains there for several weeks, or until serum ferritin concentrations indicate that almost all the stored iron has been removed (ferritin less than 12 micrograms/L). Here, concentrations of ferritin in serum were used as an index to iron overload and removal of stored iron. We report changes in hemoglobin, serum ferritin, iron, and total iron-binding capacity during the course of removing by phlebotomy more than 20 g of iron from a patient with idiopathic hemochromatosis.

Hepatic and serum ferritin concentrations in patients with idiopathic hemochromatosis

Hepatic iron and ferritin concentrations have been measured in needle biopsy specimens from patients with idiopathic hemochromatosis and from patients with other liver diseases. There was an excellent correlation between liver iron and ferritin concentrations in patients with miscellaneous liver diseases, but this was not found for the patients with hemochromatosis either before or after treatment. The proportion of liver iron bound to ferritin was lower in treated and untreated hemochromatosis than in the other patients. This probably reflects the formation of increasing amounts of hemosiderin with increasing iron deposition. Three patients in the early stage of idiopathic hemochromatosis were studied. These patients had high concentrations of hepatic iron and ferritin, but had serum ferritin concentrations within, or just above, the normal range. These results suggest that, in the early stage of hemochromatosis, there is no failure of ferritin synthesis in the liver and that normal levels of serum ferritin are present either because the total body iron content is within the normal range or because the liver parenchymal cells are not, in the absence of liver damage, an important source of plasma ferritin.

Treatment of iron storage disorders.

Iron metabolism in man is characterised by a limited exchange with the external environment and an efficient reutilisation of iron within the body. In normal subjects, the daily absorption from the gut is balanced by an equivalent small daily loss from the body of approximately Img. Although iron exchange with the environment is slight under physiological conditions, in disease states the homeostatic mechanism may be disturbed, with consequent iron deficiency or iron overload. Iron losses cannot compensate for abnormal increases in either oral or parenteral iron since no major excretory pathway for iron exists in man; the inevitable result is an increase in body iron content. Iron supplies surplus to physiological requirements are stored as haemosiderin in macrophages of the spleen, liver and bone marrow, and also as ferritin within parenchymal cells of the liver, muscle, and other organs. Sequestration of iron within the large ferritin moleculealso protects against the damaging effects of iron. In the normal, ironreplete subject, approximately 35 % of the total body iron is present as storage iron. This provides an internal reserve which can be mobilised when iron requirements exceed the amount absorbed, such as in pregnancy. Iron overload may be produced by 3 possible mechanisms: