Deficiency iron metabolism

Attention to iron metabolism is particularly important in women for the reason mentioned above. Additionally, in pregnancy, allowances must be made for the growing fetus. Older people with poor dietary habits ( tea and toasters ) may develop iron deficiency. Iron deficiency anemia due to inadequate intake, inadequate utilization, or excessive loss of iron is one of the most prevalent conditions seen in medical practice. 

Fluxes of iron from the plasma towards BM and other tissues can be quantified by ferrokinetic studies, using 59Fe and sophisticated computer models (Ricketts et ah, 1975 Ricketts and Cavill, 1978 Barosi et ah, 1978 Stefanelli et ah, 1980). Plasma iron turnover (PIT), erythroid iron turnover (EIT), non-erythroid iron turnover (NEIT), marrow iron turnover (MIT), and tissue iron turnover (TIT) could be calculated in many disorders of iron metabolism and in all kinds of anaemias. Iron is rapidly cleared from the plasma in iron deficiency and in haemolytic anaemias. If more iron is needed for erythropoiesis, more transferrin receptors (TfR) are expressed on erythroblasts, resulting in an increased flux of iron from intestinal mucosal cells towards the plasma. In haemolytic anaemias MPS, and subsequently hepatocytes, are overloaded. In hereditary haemochromatosis too much iron is absorbed by an intrinsic defect of gut mucosal cells. As this iron is not needed for erythropoiesis,... 

Although many animal models for iron overload exist, some mimicking certain aspects of HH, the 32-microglobulin knockout mouse is of special interest as it revealed for the first time crucial aspects of the pathogenesis of human HH in an animal model, and also because it underlines the important links between iron metabolism and the immune system. Hepatic iron overload in 32-microglobulin ( 32m)-deficient mice appeared to be similar to that found in HH, with pathological iron depositions occurring predominantly in liver parenchymal cells (de Sousa et ah,... 

Iron is an extremely important element present in all living organisms correspondingly, iron metabolism is well studied. Both iron deficiency and iron excess are origins of serious pathologies (iron-deficit anemias, hereditary hemochromatosis, thalassemia, etc.) associated with the overproduction of oxygen radicals. Free radical-mediated processes, characteristic of these pathologies, are considered in Chapter 31 here we will look at some mechanisms of toxic effects of iron. 

There are numerous in vitro and in vivo studies, in which the damaging free radical-mediated effects of iron have been demonstrated. Many such examples are cited in the following chapters. However, recent studies [170,171] showed that not only iron excess but also iron deficiency may induce free radical-mediated damage. It has been shown that iron deficiency causes the uncoupling of mitochondria that can be the origin of an increase in mitochondria superoxide release. Furthermore, a decrease in iron apparently results in the reduction of the activity of iron-containing enzymes. Thus, any disturbance in iron metabolism may lead to the initiation of free radical overproduction. 

Reduced food intake and efficiency of food use, altered iron metabolism, clinical signs of copper deficiency. Onset of puberty delayed 10 weeks, decreased conception rate (fertility 12-33% vs. 57-80% in controls), disrupted estrus cycle (67% were anestrus vs. 7% in controls), and other signs consistent with decreased releases of luteinizing hormones associated with altered ovarian secretion (3, 4) Growth and fertilization normal liver copper 10 mg/kg DW only 16% of embryos developed normally (2)... 

Alcohol indirectly affects hematopoiesis through metabolic and nutritional effects and may also directly inhibit the proliferation of all cellular elements in bone marrow. The most common hematologic disorder seen in chronic drinkers is mild anemia resulting from alcohol-related folic acid deficiency. Iron deficiency anemia may result from gastrointestinal bleeding. Alcohol has also been implicated as a cause of several hemolytic syndromes, some of which are associated with hyperlipidemia and severe liver disease. 

Wilson, J. F., Lahey, M. E. and Heiner, D. C. 1974. Studies on iron metabolism. V. Further observations on cow s milk-induced gastrointestinal bleeding in infants with iron-deficiency anemia. J. Pediatr. 84, 335-344. 

Anemia may result from other complications even when iron supply is sufficient. A decrease in hemoglobin synthesis, a fault in transport mechanisms or destruction of erythrocytes have all been noted. Sideroblastic or iron-loading anemias are characterized by a fault in iron metabolism (see Section 62.2.3.2). There are also several other syndromes of iron deficiency known clinically, including pica and Goodpasture s syndrome (an immune-related lung and kidney disease). The different categories of anemia have been discussed in detail by Prasad.48... 

Copper is required for the activity of enzymes associated with iron metabolism, elastin and collagen formation, melanin production and the integrity of the central nervous system. It is required with iron for normal red blood cell formation. Copper is also required for bone formation, brain cell and spinal cord structure, the immune response and feather development and pigmentation. A deficiency of copper leads to poor iron mobilization, abnormal... 

No substances containing only a single hydroxamic acid bond have thus far been isolated from natural materials as the metal complex. They are included here, however, in view of the known affinity of even monohydroxamic acids for iron (2) and also because some are related to higher hydroxamates for which a role in iron metabolism seems assured, l us-arinine, for instance, is both a constituent of ferrirhodin and is produced at high levels in iron deficiency. Although the structures are quite varied they are, for the most part -- like the di- and tri- hydroxamates — derived from the N-hydroxyamino acids. 

In addition to the role of flavoproteins in iron metabolism, it is possible that the anemia associated with riboflavin deficiency is a consequence of the impairment of vitamin Be metabolism in riboflavin deficiency. Pyridoxine oxidase is a flavoprotein and, like glutathione reductase, is very sensitive to riboflavin depletion (McCormick, 1989). Vitamin Be deficiency can result in hypochromic anemia as a result of impaired porphyrin synthesis. Although riboflavin depletion decreases the oxidation of dietary vitamin Be to pyridoxal (Section 9.2), it is not clear to what extent there is secondary vitamin Be deficiency in riboflavin deficiency This is partly because vitamin Be nutritional status is commonly... 

---