Iron-deficiency anemia is probably the commonest deficiency disease in infants and children throughout the world today. This prevalence is indeed surprising as the condition can be readily detected. Moreover, iron medication is cheap and for many years has been known to be effective in the prephylaxis and treatment of iron-deficiency anemia. In America, reportedly the most health-conscious of all countries, Guest and Brown (1957) have reported that the incidence, in at least one centre, is as high today as it was twenty years ago. If this is true in a country where practicing physicians are well primed about the importance of adequate nutrition, it is likely that in less-privileged communities there is probably greater failure to recognize or correct this deficiency state.

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Iron deficiency is one of the most common nutritional disorders worldwide. It is especially serious during pregnancy with serious health consequences for both the mother and her developing fetus. In humans these include fetal growth retardation, impaired cognitive development and premature birth. In rats, the pups born to iron deficient mothers are smaller, with changes in liver and heart size. As adults, the offspring develop hypertension and obesity. Why these changes occur is not clear. One possible hypothesis is that iron deficiency changes the cell membrane. I aimed to investigate this hypothesis, using an in-house iron deficient maternal rat model, designed by our group, additionally I have designed an iron deficient human liver hepatoma cell line model (HepG2). The effect of iron deficiency on maternal and neonatal erythrocytes membranes was tested. Iron deficiency significantly increased the mothers’ erythrocytes sensitivity to low osmotic pressure. In contrast, the neonates’ erythrocytes sensitivity was not affected by iron deficiency. The effect of iron deficiency on membrane protein profile was also studied in maternal and neonatal liver total membrane proteins, using proteomics analysis. Mitochondrial proteins were the most affected, especially in neonates. Whole cell patch clamp recording was used to study the effect of iron deficiency on the membranes’ electrophysiological properties. HepG2 cells had linear current-voltage relationships between -130 and +60 mV. Furthermore iron deficiency reduced the membranes’ input resistance reflected by an increase in holding current and in slope conductance. These changes were not reversed by K+ channel blockers (Ba2+ and quinine) suggesting no change in K+ channel protein expression. Interestingly and unexpectedly it increased the change in conductance, Sr2+ had a similar effect. Therefore iron deficient membranes had increased permeabilit

Graduation date: 1980

Thesis (M.S.)--Eastern Illinois University, 2007. / Includes bibliographical references (leaves 46-51).

Corrigenda tipped to title page. / Includes bibliographical references (leaves 313-353). / xxvii, 353 leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Investigates the iron status and dietary intakes in 6-24 month old children in Australia and Ghana and assesses the effects of dietary calcium on intestinal iron absorption. The true prevalence of non-anaemic iron deficiency (NAID) and iron deficiency anaemia (IDA) and dietary intakes in infants and toddlers from a broad socio-economic background were assessed by haematological and biochemical parameters, semi-quantitative diet recall and anthropometric measurements. The high prevalence of iron deficiency and anaemia found in Australian and Ghanaian children can be attributed to the low intake of bioavailable iron in weaning diets which are often ingested with large amounts of calcium. While calcium has been shown to inhibit the absorption of iron, its mechanism of interaction with iron absorption at the intestinal level is not known. The rat was used as an experimental model to investigate the effects of dietary calcium on duodenal iron uptake. The results indicate there is a critical period during weaning when the consumption of high dietary calcium with low iron can retard growth potential. Dietary calcium significantly inhibits non-haem iron absorption at the intracellular level by up-regulating villus enterocyte ferritin concentrations under iron deficiency conditions. / Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Science, 1998

Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Science, 1998? / Corrigenda tipped to title page. Bibliography: leaves 313-353.

Corrigenda tipped to title page. Bibliography: leaves 313-353. This study investigated the iron status and dietary intakes in 6-24 month old children in Australia and Ghana and assessed the effects of dietary calcium on intestinal iron absorption. The true prevalence of non-anaemic iron deficiency (NAID) and iron deficiency anaemia (IDA) and dietary intakes in infants and toddlers from a broad socio-economic background were assessed by haematological and biochemical parameters, semi-quantitative diet recall and anthropometric measurements. The high prevalence of iron deficiency and anaemia found in Australian and Ghanaian children can be attributed to the low intake of bioavailable iron in weaning diets which are often ingested with large amounts of calcium. While calcium has been shown to inhibit the absorption of iron, its mechanism of interaction with iron absorption at the intestinal level is not known. The rat was used as an experimental model to investigate the effects of dietary calcium on duodenal iron uptake. The results indicate there is a critical period during weaning when the consumption of high dietary calcium with low iron can retard growth potential. Dietary calcium significantly inhibits non-haem iron absorption at the intracellular level by up-regulating villus enterocyte ferritin concentrations under iron deficiency conditions.

Thesis (M.S.)--California Polytechnic State University, 2008. / Mode of access: Internet. Title from PDF title page; viewed on April 20, 2009. Major professor: Susan Hawk, Ph.D., R.D. "Presented to the faculty of California Polytechnic State University, San Luis Obispo." "In partial fulfillment of the requirements for the degree of Master of Science in Agriculture, with Specialization in Food Science and Nutrition." "August 2008." Includes bibliographical references (p. 72-78). Also available on microfiche.