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).

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.

Thesis (M.S.)--West Virginia University, 2004. / Title from document title page. Document formatted into pages; contains v, 54 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 34-36).

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This thesis investigates possible mechanisms underlying the decreased kidney size and the development of high blood pressure in the offspring of our model of maternal iron deficiency. This study has demonstrated that a maternal iron deficient diet has no effect on gene expression of either markers of vasculogenesis/angiogenesis or regulators of apoptosis and cell proliferation in the kidneys of the offspring. The effect of maternal iron deficiency on well documented mechanisms involved in blood pressure regulation were investigated in the offspring. The data showed that neither renal sodium transport nor nephron number are involved in hypertension development in our model of maternal iron deficiency. The renin angiotensin system showed significant increase in the renal renin mRNA expression, and pulmonary ACE1 mRNA and activity levels in newborn offspring of iron deficient mothers.  These changes are unique for maternal iron deficiency as they have not been seen in the other models of nutritional programming.  However, they are also temporary and disappear by two weeks after birth and at this stage it is unknown if and how the renin angiotensin system contributes to hypertension development in the offspring of iron deficient mothers. Finally, the whole rat genome arrays were used to identify new genes and pathways affected by maternal iron deficiency in fetal kidneys.  The results of the microarray experiment suggested renal inflammation and increased collagen cross-linking leading to stiffening of vascular walls, as possible causes of hypertension in the offspring of iron deficient mothers.  Further analysis showed, however, that both mechanisms do not appear to be involved.  The microarray study also identified CD36 scavenger receptor as being significantly up-regulated in the kidneys of the fetuses of iron deficient mothers, but its expression significantly decreased in adult animals compared to controls. The data presented in this thesis indicate that the effect of an iron deficient diet on offspring blood pressure is multifactorial and complex.

Thesis PlanA (M.S.)--University of Wisconsin--Stout, 2009. / Includes bibliographical references.

Thesis--M. Med. Sc., University of Hong Kong, 1984.

Thesis (M.S.)--West Virginia University, 2003. / Title from document title page. Document formatted into pages; contains vii, 56 p. Vita. Includes abstract. Includes bibliographical references (p. 41-45).