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Inflammatory disorders are associated with a decrease in iron absorption because of the blockade of iron in storage organs. Fish oils, rich in n-3 PUFA, are used to prevent and treat inflammatory disorders and increase iron absorption in noninflamed rats. Here we examine whether n-3 PUFA prevent inflammation-related hypoferremia. Two groups of rats were fed isoenergetic semipurified diets (a standard diet and a sardine oil-rich diet). A carrageenan granuloma was induced in half of the rats of each dietary group. Ferrokinetic studies using 59Fe, hematological analyses, and iron store evaluation were performed in noninflamed and inflamed rats. Although dietary n-3 PUFA increased 59Fe absorption in carageenan-treated rats, they did not restore the hypoferremia associated with inflammation, which is due to several mechanisms. Among these mechanisms, the blockade of iron in storage organs is relevant. However, this blockade was less evident in the spleen of inflamed rats fed the sardine oil diet.

The objective of the present study was to examine the effects of fish oil (FO)- and olive oil (OO)-rich diets on Fe metabolism and oxidative stress. Rats were fed for 16 weeks with diets containing 50 g lipids/kg; either OO, maize oil (MO) or FO. OO or MO diets contained a standard amount (100 mg/kg) of all-rac-alpha-tocopheryl acetate. FO diets were supplemented with 0, 100 or 200 mg all-rac-alpha-tocopheryl acetate/kg (FO-0, FO-1 or FO-2 diets, respectively). At the end of the feeding period, we measured non-haem Fe stores in liver and spleen, and erythrocyte and reticulocyte count. We also determined antioxidants and products derived from lipid peroxidation in plasma and erythrocytes. Our results showed reduced non-haem Fe stores in rats fed any of the FO diets. Reticulocyte percentage was higher in the rats fed FO-0 and FO-1. Plasma alpha-tocopherol was very low in rats fed the FO-0 diet. Rats fed the FO-1 and FO-2 diets showed higher alpha-tocopherol in plasma than the FO-0 group but lower than the MO or OO groups. We did not observe such differences in the alpha-tocopherol content in erythrocyte membranes. Superoxide dismutase and glutathione peroxidase activities were lower in the erythrocytes of rats fed the FO-0 diet. The products derived from lipid peroxidation were also higher in the FO groups. The administration of FO-rich diets increased lipid peroxidation and affected Fe metabolism. On the other hand, the OO-rich diet did not increase oxidative stress and did not alter Fe metabolism. Based on these results, we conclude that FO supplementation should be advised carefully.

We studied the influence of the fatty acid composition of three different diets on iron absorption in relation to the lipid peroxidation of the erythrocyte membranes. After weaning, three groups of rats were fed isoenergetic semipurified diets for 16 wk: control diet (containing canola oil and peanut oil), tripalmitin diet (a saturated fatty acid diet) and a sardine oil diet rich in polyunsaturated fatty acids. Eight rats from each group were administered 59FeSO4 by gastric intubation for ferrokinetic studies, and six rats from each group were used for several analyses in blood, liver, spleen and erythrocytes. Results obtained from 59Fe eliminated in feces and 59Fe present in plasma, both calculated by the area under the curve and from maximum concentration in plasma, indicated that the sardine oil diet induced higher iron absorption than the control diet. The lipid peroxidation of erythrocyte membranes in rats fed sardine oil was higher than that in control rats due to high membrane's (n-3) polyunsaturated fatty acid content and low alpha-tocopherol level. The 59Fe in liver and spleen of rats fed the sardine oil diet was higher than in rats fed the control diet, and 59Fe was diverted to erythrocytes to a greater extent than in rats fed the control diet due to their reduced life-span. The sardine oil diet, by lessening alpha-tocopherol and raising the degree of lipid peroxidation in erythrocytes, augments iron absorption, whereas the tripalmitin diet, by protecting erythrocyte membranes from lipid peroxidation, leads to a lower rate of iron absorption.

Iron overload induces a rise in lipid peroxidation, but there are no data on the effects of iron administered in vivo on the production of free radicals by inflammatory cells. Further, there is lack of agreement about the benefits of deferoxamine (Dfx) in the treatment of anemia and oxidative stress during inflammation and chronic diseases. In this study, iron-dextran (Fe-dextran) or Dfx was administered subcutaneously during the acute and chronic phases of carrageenan-induced granuloma. Several parameters related to iron metabolism, inflammatory cell activity, and lipid peroxidation were measured in liver, plasma, and the inflammatory exudate. Treatment with Fe-dextran increased iron content in plasma and in stores, increased production of superoxide anion (O2-) by inflammatory cells and lipid peroxidation, and also altered the inflammatory process. Dfx mobilized iron from stores without modifying essential parameters related to anemia or to the level of lipid peroxidation induced by inflammation. We conclude that treatment with Fe-dextran had a beneficial effect on recovery from the anemia of inflammation. Nevertheless, the high levels of loosely-bound iron found after Fe-dextran treatment in plasma and in exudate contribute to the increase in oxidative stress. Dfx treatment had no effect on anemia or on lipid peroxidation.

We studied the effect of dietary lipids on iron metabolism and lipid peroxidation during induced adjuvant arthritis and/or iron overload in rats. We compared a control diet containing corn oil and rapeseed oil with a diet devoid of polyunsaturated fatty acids containing only tripalmitin as lipids. Four subgroups of rats were used with each diet: without further treatment, with induction of adjuvant arthritis, with iron overload, and with induction of adjuvant arthritis and iron overload. The profile of fatty acids present in plasma and in microsomes changed in rats fed the tripalmitin diet. The level of tetra- and pentaunsaturated fatty acids was reduced, and the level of monounsaturated fatty acids and iron stores was increased with respect to control rats. Thus, ingestion of a tripalmitin diet reduced the substrate for lipid peroxidation, as shown by the decrease in thiobarbituric acid-reactive substances in plasma and conjugated dienes in hepatic microsomal fraction. Adjuvant arthritis and iron overload had a synergistic effect on lipid peroxidation and iron storage in liver. Further, in the hepatic microsomal fraction, tripalmitin reduced the levels of cytochrome P-450, and arthritis reduced the levels of cytochrome P-450 and Ca2+ sequestration. Our results suggest that rats fed tripalmitin showed a reduction of lipid peroxidation induced by inflammation or by iron overload, because of the lack of polyunsaturated fatty acids in the diet, although tripalmitin usually increases the iron stores in the body and causes hepatic alterations.

Iron (Fe) absorption by three segments (duodenum, jejunum, and ileum) of the small intestine of chickens was studied by a perfusion technique in vivo in closed circuit using 59Fe Cl3 and was related to the histological characteristics of each segment. The serosal transfers of Fe for the duodenum and jejunum were the same (14%/cm), but significantly different (p < 0.05) from those of the ileum (9%/cm), which may be explained by the morphological and histological properties of the gut of chickens. However, the presence of Fe in blood and in liver was significantly lower after perfusion of the jejunum and ileum than after perfusion of the duodenum. It is concluded that chickens show an early adaptation of small intestine to Fe absorption in response to the considerable loss of Fe suffered during the laying process.

Sprague-Dawley rats were fed for 4 months on a control diet or a polyunsaturated-fatty-acid (PUFA)-deficient diet. The combined effects of iron overload (Fe dextran) or Fe deficiency (desferrioxamine) on carrageenan-induced granuloma were studied. PUFA deficiency induced changes in Fe metabolism, but no alterations in lipid peroxidation variables were observed. Inflammation implied an increase in lipid peroxidation, Fe storage and caeruloplasmin concentration, together with symptoms of anaemia. PUFA deficiency in inflamed rats gave rise to a lower inflammatory response (granuloma weight and prostaglandin E2 concentration) and ethane exhalation. Fe overload potentiated inflammatory and lipid peroxidation processes, whereas Fe deficiency decreased them.

We have used the carrageenan-induced pouch-granuloma in rats to investigate how changes in low-molecular-mass iron chelate levels in the exudate, induced by iron loading (iron-dextran) or chelation (desferrioxamine) influence cellular and systemic inflammatory parameters. In the iron-treated group we observed a rapid decrease in the number of leukocytes and exudate volume; there was also an increase in ferritin iron and low-molecular-mass iron chelates, and on the eighth day a systemic response. In the desferrioxamine-treated group we detected a decrease in low-molecular-mass iron chelates, ferritin iron, and an increase in the number of leukocytes. We describe the protective effects of desferrioxamine against the deleterious effects of ferrous iron and relate this to its chelating and scavenging activity. The results suggest that the levels of low-molecular-mass iron chelates modulate the inflammatory response, possibly through their contribution to the oxygen free radical generation, which is responsible for the cell membrane damage and subsequently its death. The modulatory action of iron-dextran and desferrioxamine support our hypothesis.

1. Haematological values and iron content in liver, spleen, kidneys and intestine were determined in Shaver chickens of both sexes at 4, 8, 13 and 18 weeks and in females at 24 weeks (the beginning of the laying period). 2. The haematocrit decreased significantly in laying compared with non-laying females and the haemoglobin concentration was similar to that in the prelaying state. Plasma iron in laying females increased to four times the basal value at 13 weeks. 3. Females of 13 and 18 weeks (prelaying state) stored more iron than males at the same age. A simultaneous liver and spleen mobilisation of stored iron and increased intestinal iron accumulation took place in the laying process. The haematological variables examined were minimally altered. 4. The iron contents of both heart and kidneys were influenced by age and followed a linear trend, except that in the heart of females where a quadratic response was observed.

We have studied some hematological parameters and iron and ferritin iron contents in different organs of New Hampshire chickens at the ages of 4, 8, 13, and 18 wk for both sexes, as well as 24 wk for laying hens, in order to study the variations with age, the existence of sex differences, and the accommodations to laying. The hematocrit and hemoglobin levels did not show important variations, but plasma iron increased at laying. The iron and ferritin iron concentrations in liver and spleen increased more slowly during growth than the total iron and ferritin iron contents, and no significant decline was observed at laying. The iron concentration in the heart and pectoral muscle stayed constant throughout the period studied, and kidneys showed slight increase with age. However, the iron concentration in the intestine decreased from the proximal to the distal segments and also increased in the duodenum at laying. No differences caused by sex have been detected in the organs studied. The absence of differences caused by sex in the organ iron stores in favor of females, especially in liver, and the lack of influence of the laying process in iron stores could be a consequence of the low laying frequency of this strain.

Iron has been implicated in the inflammatory process. In this paper we studied the modulating inflammatory activity of iron in the carrageenan-induced granuloma pouch, taking indometacin as a standard anti-inflammatory drug. Sprague-Dawley rats were injected subcutaneously with desferrioxamine (100 mg/kg) and indometacin (5 mg/kg) for 3 consecutive days before granuloma induction, followed by a daily administration in the granuloma pouch until the day before death. We determined the granuloma weight and assayed in the exudate: volume, number of leukocytes, PGE2 levels and loosely bound iron content at 1 (acute inflammation) and 6 days (chronic inflammation) after granuloma induction. Our results show a dual effect of desferrioxamine, inflammatory in the acute phase and anti-inflammatory in the chronic phase. These results are discussed in relation to chemotaxis and to the potential role of iron on oxygen free radical production, collagen synthesis and hydroperoxide generation, while indometacin acts through the cyclooxygenase pathway.

The effect of acute, subchronic, and chronic experimental models of inflammation upon hematocrit, hemoglobin, serum iron and ferritin iron and nonheme iron concentration in the liver and spleen has been studied in the rat. In the acute model (carrageenan oedema) no iron mobilization took place, whereas in the chronic models differences in iron mobilization were observed, related to their different chronicity and to the time elapsed from induction. The carrageenan-induced granuloma (from 12 h to 8 days) (subchronic model) was accompanied by a decrease of plasma iron (12 and 24 h), a later decrease of the hematocrit values (2 and 4 days) and high ferritin and nonheme iron concentrations in the liver and spleen for 4 days, followed by a tendency to return to the control values. The anemia in the adjuvant arthritis (from 1 to 4 weeks after induction) (chronic model) was observed at 7 days and is related to increased iron stores in the liver and spleen. However, the iron store levels in liver decreased and fell later below control values. The increase of ferritin and nonheme iron concentrations may be responsible for the reduced availability of iron release from tissue.

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. The iron content in internal organs in shaver was higher than in New Hampshire. 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. 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. 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. Iron data obtained in the present paper reflect the specific genetic adaptation to egg production of the shaver strain.