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Iron deficiency during pregnancy has many effects on both the mother and her developing foetus. These can be both short and long term. One effect is an alteration in fatty acid metabolism and we hypothesised that these changes may result in alterations in membrane function and structure. In order to test this hypothesis, we measured osmotic sensitivity in red blood cells isolated from neonates and their mothers at different times following birth. We fed female rats control or iron-deficient diets for 4 weeks prior to mating and kept them on the same diet until term. At that time, we returned one group of deficient dams to the control diet. The others were kept on the same diet. We showed that iron deficiency results in a decrease in osmotic sensitivity in the mothers but not in their neonates. Returning the dams to the control diet resulted in a return of their red cell osmotic sensitivity to control levels. In the neonates, there was no recovery in haematocrit or in any other parameter, though they did not get any worse, in contrast to the pups being suckled by deficient mothers. The data show two things. The first is that following birth, the mother restores her own iron stores at the expense of the pups, and secondly, there are differences in properties and sensitivities between red cells from mothers and their neonates. This latter observation cannot be explained by differences in the membrane fatty acid profiles, which were not significantly different.

Iron and copper homeostasis have been studied in various tissues after iron-loading with the polynuclear ferric hydroxide carbohydrate complexes, iron dextran, iron polymaltose, iron sucrose and iron gluconate for four weeks. There were significant increases in the iron content of the different rat tissues compared to controls, with the exception of the brain, which showed no change in its iron content following iron loading. However, the level of iron loading in the different tissues varied according to the preparation administered and only iron dextran was able to significantly increase the iron content of both broncho-alveolar macrophages and heart. The hepatic copper content decreased with iron loading, although this did not reach significance. However the copper content did not alter in the iron loaded broncho-alveolar macrophages. Despite such increases in hepatic iron content, there was little evidence of changes in oxidative stress, the activities of cytosolic (apart from iron dextran) or mitochondrial hepatic superoxide dismutase, SOD, were similar to that of the control rats, confirming the fact that the low reduction potential of these compounds prevents the reduction of the ferric moiety. It was not necessary for macrophages to significantly increase their iron content to initiate changes in NO* release. Iron gluconate and iron sucrose increased NO* release, while iron polymaltose and iron dextran decreased NO* release although only the latter iron preparation significantly increased their iron content. It may be that the speciation of iron within the macrophage is an important determinant in changes in NO* release after ex vivo stimulation. We conclude that tissues loaded with iron by such polynuclear iron complexes have variable loading despite the comparable iron dose. However, there was little evidence for participation of the accumulated iron in free radical reactions although there was some evidence for alteration in immune function of broncho-alveolar macrophages.

During pregnancy, iron is transferred from the mother to the fetus across the placenta. The mechanism has been extensively studied. Altered iron metabolism changes transfer, but also has other consequences. In this review, we examine how the placenta adapts to altered iron supply, both in terms of changing cytokine expression and in relation to the proteins of iron transfer. Changing iron levels alters the levels of other metals, especially copper, and we review how this is related to changing function. There are also consequences to the placenta itself, to vascularisation and other aspects of the physiology. In turn, this has effects on the fetus and we review how growth and development are modified. Finally, we examine in more detail the efflux process, how it is regulated and, especially, the putative role of the placental Cu oxidase in the efflux process. As appropriate, we draw on data from humans, from animal models and from cell culture systems to illustrate the information.

Sarcoplasmic reticulum has been isolated from the white muscle of 15 species of teleost fish adapted to diverse thermal environments. Evidence has been obtained that the Ca2+-dependent ATPase of fish sarcoplasmic reticulum has undergone evolutionary modification for function at different temperatures. Compared with tropical fish, cold adapted species have higher rates of Ca2+ transport and Ca2+-ATPase activities at low temperatures. Most species have linear Arrhenius plots over the temperature range 0–30°C. Activation enthalpies (ΔH ≠) of the ATPase ranged from 53–190 kJ mol−1 and were positively correlated with environment temperature. Activation entropy (ΔS ≠) varied from negative values in cold adapted species to positive values in tropical fish. In contrast to the Ca2+-ATPase, the “basal” ATPase of fish sarcoplasmic reticulum showed no relationship between either ATPase activity or thermodynamic activation parameters and environmental temperature. Only the Ca2+-dependent ATPase is coupled to Ca2+ transport. The percentage of “total” ATPase activity which is Ca2+ activated is higher at low temperatures in cold than in warm adapted species. For example, ratios of Ca2+-dependent/total ATPase at 2°C varied from 80–98% in Arctic, Antarctic and North Sea species to only 2–50% in various tropical fish. Above 20°C, similar ratios in the range 80–98% were obtained for all species. The nature of the “basal” ATPase and mechanisms of temperature adaptation of fish sarcoplasmic reticulum are discussed.