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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were made to determine the neutrophil's phagocytosis and bactericidal function in three groups of rats (control, iron deficiency, and iron supplement). Results showed that there were significant differences in values of chemiluminescence (CL) among three groups. The values of peak CL and five minutes integrated CL were markedly decreased in neutrophils of iron-deficient rats, accounting for only 41% and 32% of the control's values respectively. These suggested that the activity of NADPH oxidase was decreased, and the function of respiratory burst of neutrophils was impaired. The activity of myeloperoxidase in the iron-deficient neutrophils was also significantly lower than that in the control cells. It constituted only 30% of the control's value, indicating that the bactericidal function of neutrophils was injured. One week after iron administration, the low values of the peak CL, the five minutes integrated CL and the activity of myeloperoxidase all went up apparently, but not reached the normal levels yet. The time the function of neutrophils in iron-deficient rats returned to normal may be related to the process of neutrophil maturation in bone marrow.
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PMID:[Investigation of impairment of neutrophil's phagocytosis and bactericidal function in rats with iron deficiency]. 166 Aug 47

A Technicon H-1 hematologic analyzer was used to measure the mean leukocyte myeloperoxidase (MPX) in 160 patients seen in a hematology clinic. The normal range was -15 to +10, which included 95% of 300 consecutive hospitalized patients. No abnormalities in the MPX were found in 35 patients with beta-thalassemia minor, 8 with iron deficiency, 14 with myeloproliferative disorders, 17 with autoimmune disorders, and 37 patients with lymphoma in complete remission. On the other hand 36% (10/28) of lymphoma patients with active disease either at diagnosis or relapse had a MPX of greater than 10 compared to only 2.3% (7/300) in hospitalized patients (P less than 0.001). Increased levels of MPX were found primarily in patients with non-Hodgkin's lymphoma (NHL) of intermediate or high grades, or Hodgkin's disease [56% (9/16) compared to only 8.3% (1/12) in those with low grade NHLs, P less than 0.05]. The MPX levels returned to normal after successful treatment. Of the various chemotherapeutic agents used, only hydroxyurea led to a consistent elevation of the MPX. The authors conclude that MPX is commonly increased in patients with lymphoma and in those receiving hydroxyurea. Further studies are required to determine if the MPX is a sensitive test for relapse in patients with lymphomas who had an elevated pretreatment value.
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PMID:The mean leukocyte myeloperoxidase index in hematological patients. 255 19

The polymorphonuclear granulocyte (PMN) kills ingested bacteria by mechanisms that include myeloperoxidase (MPO) and a sudden increase in oxygen consumption (the oxidative burst), both of which are iron dependent. The magnitude of the oxidative burst and activity of MPO were determined in PMNs during the progression of iron deficiency (ID) and following its treatment in rats. As ID developed, the oxidative burst after zymosan activation was less depressed than the activity of MPO. There was no change in the oxidative burst after activation with phorbol myristate acetate (PMA) or in the generation of superoxide (O2-) by NADPH oxidase-containing particles from PMNs. Following iron treatment, impairment of the oxidative burst after zymosan activation was corrected after 1 day. In contrast, the deficit in MPO activity was not corrected until 7 days after initiation of iron treatment. The pattern of recovery in MPO activity after iron treatment corresponded to the prolonged period of maturation of the PMN primary granule since the formation of primary granules, which contain MPO, takes place only in the early, mitotic stages of maturation. The tendency of the PMN to maintain the oxidative burst allows the cell to preserve its capacity for bacterial killing during the progression of iron deficiency.
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PMID:Iron deficiency and neutrophil function: different rates of correction of the depressions in oxidative burst and myeloperoxidase activity after iron treatment. 303 7

We developed a clear-cut nutritional iron deficiency anemia without concomittant malnutrition in rats given a low iron diet, and we restored normal iron and hemoglobin levels in these same animals with iron dextran injections. The neutrophil function studies performed during and after a period of iron deficiency showed the following: Phagocytosis of Staphylococcus aureus 502A, Streptococcus pneumoniae, and Salmonella typhimurium was not altered by iron deficiency or by the administration of iron; phagocytosis of Candida albicans was moderately abnormal during iron deficiency, and became normal with the restoration of iron sufficiency. Microbicidal activity towards Staphylococcus aureus 502A and Candida albicans, two catalase-positive microorganisms, was markedly decreased (to 50% of control values) and returned to normal when iron sufficiency was restored. Killing of a catalase-negative organism, Streptococcus pneumoniae was normal in iron-deficient rats. This pattern of differential bactericidal activities suggested an abnormality of the oxidant radical-generating machinery in neutrophils of iron-deficient animals. Indeed, iron deficiency caused a marked decrease of neutrophil nitroblue tetrazolium dye reduction, which disappeared after iron administration. Neutrophil myeloperoxidase activity was slightly decreased in iron deficient rats and returned to normal after iron administration. Microbicidal activity towards a gram-negative, catalase-positive organism, Salmonella typhimurium, was equal in iron deficient and iron sufficient animals. Our combined results suggest that a definite microbicidal defect is the consequence of nutritional iron deficiency, apart from any protein-calorie malnutrition. This defect affects the disposal in PMNs of two catalase-positive microorganisms (which require intracellular production of oxidant radicals for their destruction) but not of a catalase-negative bacterial species.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neutrophil bactericidal dysfunction towards oxidant radical-sensitive microorganisms during experimental iron deficiency. 608 85

Studies were performed to determine the effects of iron deficiency in the rat on neutrophil activation and on levels of neutrophil myeloperoxidase and cytochrome b. The period of time required for neutrophil activation was not significantly affected by iron deficiency, but the maximum rates of respiration attained after activation were markedly lower (60% decrease) in iron-deficient neutrophils than in control cells. The myeloperoxidase activity of neutrophils from iron-deficient rats was also markedly decreased (approximately 75%) compared with the activity of control cells; however, the concentration of cytochrome b in the neutrophils was unaffected by iron deficiency.
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PMID:Iron deficiency in the rat: effects on neutrophil activation and metabolism. 633 Jun 57

Iron is essential for the organism. In ionized forms (Fe++, Fe ), it constitutes an integrated part of a lot of different functional proteins (Figure 1). The most important functions are participation in oxygen transport in blood, oxygen storage in muscle tissues and oxidation of nutrients in the mitochondria. Iron is an essential part of cytochrome C and alpha-glycerolphosphate dehydrogenase, and early stages of iron deficiency may, therefore, cause disturbances in tissue metabolism before development of anaemia. Thus, haemoglobin determinations is not very suitable for diagnosing early iron deficiency. The content of iron in roughages, apart from root crops (Table II), is usually sufficient to cover the requirement of domestic animals (Table III), which is met by about 50 mg per kg feed dry matter. Iron deficiency is very often caused by a reduced absorption in the intestinal tract because of components in the feed forming complexes with iron of very low solubility or inhibitors reducing the absorption processes. The immune status of the organism and its resistance against infections depends on the iron supply. Iron deficiency inhibits the myeloperoxidase activity and thus decreases the bacteriocide effect of the leucocytes. In spite of this, when exposed to infections the physiological mechanisms reduce the blood concentration of available iron. By this mode of action, invading pathogens, needing iron like the host animals, will be restrained. The low content of iron in milk (Table II) combined with a high content of iron binding lactoferrin, is ideal to protect newborn and milk fed young animals against intestinal infections.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Iron deficiency in domestic animals]. 643 95

For unknown reasons, serum ferritin levels increase in patients at risk for and with acute lung injury (ALI). To improve understanding of the relationship between serum ferritin alterations and the development of ALI, we investigated the effect of iron deficiency on the serum ferritin response of rats subjected to hemorrhage. We found that rats fed an iron-deficient diet for 6 weeks had decreased hemoglobin, hematocrit, liver total iron, liver total iron-binding capacity, and liver ferritin concentrations but the same serum ferritin concentrations as rats fed a control diet. Following hemorrhage, serum ferritin concentrations increased rapidly and progressively in rats fed a control diet. Along with increases in serum ferritin concentrations, control diet rats subjected to hemorrhage also had increased lung lavage leukocyte numbers, lung myeloperoxidase activities (lung inflammation), and lung lavage protein concentrations (lung leak) compared to control diet fed rats subjected to sham treatment. By comparison, the serum ferritin concentrations, lung inflammation, and lung leak of hemorrhaged rats fed an iron-deficient diet were decreased compared to hemorrhaged rats fed a control diet. These findings indicate that serum ferritin concentrations increase and acute lung injury develops following hemorrhage in rats fed a control, but not an iron-deficient, diet. A relatively brief exposure to an iron-deficient diet reduces hemorrhage-induced ALI.
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PMID:Serum ferritin increases in hemorrhaged rats that develop acute lung injury: effect of an iron-deficient diet. 1452 78

Iron deficiency anemia is a common feature in inflammatory bowel disease, and oral supplementation is one of the mainstay therapies. However, there is some concern that oral iron supplementation may lead to oxidative stress and exacerbation of inflammation. Our objective was to study the effect of severely deficient, moderately deficient, normal and high iron status on oxidative stress and the course of inflammation in a rat model of colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). The rats were randomly assigned to receive the low-iron diet for 3 (moderately iron-deficient group, n = 16) or 5 (severely iron-deficient group, n = 16) wk, the normal iron diet for 2 wk (normal iron group, n = 16) or the high-iron diet for 2 wk (high-iron group, n = 16). Malondialdehyde concentration, electroparamagnetic resonance measurement, myeloperoxidase activity, and histological analysis were used to evaluate oxidative stress. Noncolitic rats in the high-iron group had higher oxidative stress parameters than those in the other groups. The induction of colitis resulted in severe inflammatory changes in the high-iron and severely iron-deficient groups, and produced higher histological scores in the colon of the normal and high-iron groups. Iron overload, oxidative stress, and inflammation were lower in the moderately iron-deficient group compared with the other 3 groups. In conclusion, we suggest that low rather than normal or high iron supplementation should be considered for the treatment of iron deficiency in inflammatory bowel disease.
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PMID:Dietary iron affects inflammatory status in a rat model of colitis. 1533 12

Divalent metal transporter 1 (DMT1) is the major iron transporter responsible for duodenal dietary iron absorption and is required for erythropoiesis. Recent studies suggest that loss of DMT1 activity could be involved in metal-related lung injury, but little is known about the effects of iron status and DMT1 function on pulmonary inflammation. To better define the role of DMT1 and iron status in pulmonary inflammatory responses, we performed bronchoalveolar lavage (BAL) following intratracheal instillation of lipopolysaccharide (LPS) to the Belgrade rat, an animal model deficient in DMT1 function. In the basal state, the BAL fluid of Belgrade rats had more macrophages and higher lactate dehydrogenase, myeloperoxidase, albumin, and hemoglobin levels compared with heterozygote control rats. Following LPS instillation, the macrophage fraction relative to total BAL cell content and levels of albumin and IgM were increased in Belgrade rats compared with controls. In contrast, heterozygote Belgrade rats made anemic by diet-induced iron deficiency exhibited attenuated inflammatory responses to LPS. These combined results show that pulmonary inflammation can be modified by both DMT1 and iron status. Loss of DMT1 alters pulmonary responses necessary for lung homeostasis in the basal state and enhances LPS-induced inflammation and therefore would contribute to progression of lung injury.
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PMID:Influence of DMT1 and iron status on inflammatory responses in the lung. 2127 60

Iron deficiency is routinely treated with oral or systemic iron supplements, which are highly reactive and could induce oxidative stress via augmenting the activity of proinflammatory enzyme myeloperoxidase (MPO). To investigate the extent to which MPO is involved in iron-induced toxicity, acute (24 h) iron toxicity was induced by intraperitoneal administration of FeSO4 (25 mg/kg body weight) to MPO-deficient (MpoKO) mice and their wild-type (WT) littermates. Acute iron toxicity was also assessed in WT mice pretreated with an MPO inhibitor, 4-aminobenzoic acid hydrazide. Systemic iron administration up-regulated circulating MPO and neutrophil elastase and elevated systemic inflammatory and organ damage markers in WT mice. However, genetic deletion of MPO or its inhibition significantly reduced iron-induced organ damage and systemic inflammatory responses. In contrast to the acute model, 8 weeks of 2% carbonyl iron diet feeding to WT mice did not change the levels of circulating MPO and neutrophil elastase but promoted their accumulation in the liver. Even though both MpoKO and WT mice displayed similar levels of diet-induced hyperferremia, MpoKO mice showed significantly reduced inflammatory response and oxidative stress than the WT mice. In addition, WT bone-marrow-derived neutrophils (BMDN) generated more reactive oxygen species than MPO-deficient BMDN upon iron stimulation. Altogether, genetic deficiency or pharmacologic inhibition of MPO substantially attenuated acute and chronic iron-induced toxicity. Our results suggest that targeting MPO during iron supplementation is a promising approach to reduce iron-induced toxicity/side effects in vulnerable population.
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PMID:Myeloperoxidase deficiency attenuates systemic and dietary iron-induced adverse effects. 3021 80


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