Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the effects of iron treatment on iron deficient cross-country skiers. Kind and duration of their daily training were also considered. Forty-eight athletes were divided in three balanced groups: Group A received 160 mg ferritinic iron/die, Group B received the same amount of iron and 1 gr of ascorbic acid and Group C was untreated. Blood samples were taken at the start, after two months and four months of supplementation. Hematological and iron status parameters were determined. Average training duration was 80 min a day. Running was the most frequent method of training but also roll and country skiing were commonly used. At the initial sample low serum ferritin values were found in all the three groups (Group A = 23.3 micrograms/l, Group B = 20.9 micrograms/l and Group C = 23.5 micrograms/l). After iron treatment serum ferritin increased in Groups A and B (+67.8% and +63.6% respectively) but was slightly reduced in Group C. Serum iron was unchanged and total iron binding capacity decreased following ferritin increase. Ascorbic acid failed to increase iron absorption in Group B. A significant reduction of haptoglobin (-14% and -9% in Group A and B respectively) was also documented. We conclude that cross-country skiers extensively use running in their training and it may be one of the cause of their poor iron status. Ferritinic iron treatment seems to be effective in replacing iron stores in cross-country skiers who underwent heavy training.
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PMID:Effects of training and iron supplementation on iron status of cross-country skiers. 207 40

The ability of Haemophilus influenzae, H. parainfluenzae and H. paraphrophilus to utilize iron complexes, iron-proteins and exogenous microbial siderophores was evaluated. In a plate bioassay, all three species used not only ferric nitrate but also the iron chelates ferric citrate, ferric nitrilotriacetate and ferric 2,3-dihydroxybenzoate. Each Haemophilus species examined also used haemin, haemoglobin and haem-albumin as iron sources although only H. influenzae could acquire iron from transferrin or from haemoglobin complexed with haptoglobin. None of the haemophili obtained iron from ferritin or lactoferrin or from the microbial siderophores aerobactin or desferrioxamine B. However, the phenolate siderophore enterobactin supplied iron to both H. parainfluenzae and H. paraphrophilus, and DNA isolated from both organisms hybridized with a DNA probe prepared from the Escherichia coli ferric enterobactin receptor gene fepA. In addition, a monospecific polyclonal antiserum raised against the E. coli 81 kDa ferric enterobactin receptor (FepA) recognized an iron-repressible outer membrane protein (OMP) in H. parainfluenzae of between 80 and 82 kDa (depending on the strain). This anti-FepA serum did not cross-react with any of the OMPs of H. paraphrophilus or H. influenzae. The OMPs of each Haemophilus species were also probed with antisera raised against the 74 kDa Cir or 74 kDa IutA (aerobactin receptor) proteins of E. coli. Apart from one H. parainfluenzae strain (NCTC 10665), in which an OMP of about 80 kDa cross-reacted with the anti-IutA sera, no cross-reactivity was observed between Cir, IutA and the OMPs of H. influenzae, H. parainfluenzae or H. paraphrophilus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Utilization of enterobactin and other exogenous iron sources by Haemophilus influenzae, H. parainfluenzae and H. paraphrophilus. 215 Apr 14

Iron metabolism was studied in patients with chronic diffuse diseases of the liver. A sharp increase of ferritin content at the expense of its release from affected hepatocytes, and formation of antibodies to ferritin of the splenic type have been recorded in patients with cirrhosis of the liver. The observed growth of ferritin content in red blood cells can be explained by functional deficiency of red blood cells and by the presence of hemolytic process (twofold decrease of haptoglobin level). A conclusion has been made that ferritin content in the blood serum does not correlate with the total iron reserves, and serum ferritin level should be considered not as a sign of the pathologic process, but as an index of iron reserves capable of participating in metabolic processes.
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PMID:[Study of iron metabolism in chronic diffuse diseases of the liver]. 221 Mar 19

Effects of endurance training on O2 transport and on iron status are well documented in the literature. Only a few data are available concerning the consequences of strenuous anaerobic muscular exercise on red cell function. This study was performed to test the influence of strength training alone on parameters of red cell O2 transport and iron status. Twelve healthy untrained males participated in a strength-training programme of 2-h sessions four times a week lasting 6 weeks. After 6 weeks a small but significant reduction of haemoglobin (Hb; -5.4 g.l-1) was found (p less than 0.05). Mean red cell volume did not change, but a pronounced decrease of mean cell Hb concentration (from 329.2 g.l-1, SE 2.5 to 309.8 g.l-1, SE 1.2; p less than 0.001) and mean corpuscular Hb (from 29.6 pg, SE 0.4 to 27.7 pg, SE 0.3; p less than 0.01) was observed. Serum ferritin decreased significantly by 35% (p less than 0.01); transferrin, serum iron and iron saturation of transferrin were unaltered. Serum haptoglobin concentration was diminished significantly by 30.5% (p less than 0.01). The reticulocyte count had already increased after 3 weeks of training (p less than 0.05) and remained elevated during the following weeks. Strength training had no significant influence on the O2 partial pressure at which Hb under standard conditions was 50% saturated, red cell 2,3-diphosphoglycerate and ATP concentration as well as on erythrocytic glutamate-oxalacetate transaminase activity. The data demonstrate that mechanical stress of red cells due to the activation of large muscle masses led to increased intravascular haemolysis, accompanied by a slightly elevated erythropoiesis, which had no detectable influence on Hb-O2 affinity. Training caused an initial depletion of body iron stores (prelatent iron deficiency). Although Hb had decreased by the end of the training phase a true "sports anaemia" could not be detected.
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PMID:Consequences of 6 weeks of strength training on red cell O2 transport and iron status. 234 15

This study was undertaken to gain insight into the mechanisms responsible for the hypoferremia occurring after severe exercise. To this end, 18 athletes who were competing in a 160-km triathlon involving canoeing, cycling, and running were evaluated before the race, immediately after the finish, and thereafter at 30 min, 24 h, and 48 h. The evaluation included plasma iron, total iron-binding capacity, lactoferrin, ferritin, haptoglobin, cortisol, various enzymes, and white cell count. The cortisol, white cell count, and lactoferrin were significantly increased immediately after the race, while the plasma iron and transferrin saturation were significantly decreased. There was a 40% but nonsignificant rise in the plasma ferritin at the completion of the race, while the C-reactive protein was raised by nearly 300% at 24 h. In contrast, haptoglobin declined significantly by 24 h but was normal again 24 h later. Quantitative considerations suggested that the lactoferrin was not responsible for removing transferrin iron from circulation and hence causing the hypoferremia. Instead, it seemed more likely that the iron-related changes were occurring as part of an acute phase response initiated by muscle injury.
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PMID:Hematologic, iron-related, and acute-phase protein responses to sustained strenuous exercise. 243 98

In 110 well-trained participants of a 1000-km running competition lasting for 20 days hematological parameters, iron metabolism, and their respective changes during the race were investigated. Thirty-nine men and 11 women were accustomed to wholesome vegetarian food (lacto-ovovegetarian), 52 men and 8 women consumed a conventional western diet. In each group 50% of the runners finished the race. Before the competition started red blood cell count, hematocrit, and hemoglobin were on average below the values observed in the normal population in all groups. Both male and female runners consuming the wholesome diet showed significantly lower ferritin values than those on a western diet. During the first days of the competition hemolysis occurred leading to increased serum concentrations of bilirubin and iron and decreased haptoglobin levels. Hb concentrations showed a constant decrease during the race. Serum ferritin concentration rose about twofold within the first days and then decreased again without reaching pre-race levels. Serum iron concentrations showed a significant decrease between days 3 and 6. Iron loss was caused by hematuria (25% of all urines tested), gastrointestinal blood loss (10% of all stool specimens tested), and by sweating (4.5 micrograms iron/dl sweat). Our results suggest that especially in female long-distance runners it may be difficult to supply sufficient quantities of iron with the diet.
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PMID:Effects of long-distance running on iron metabolism and hematological parameters. 259 24

To define the hematologic changes during a mild viral infection, 93 infants were immunized with live attenuated measles virus and studied prospectively at 0, 4, 9, 14, 21, and 30 days. Hemoglobin concentration decreased significantly by days 9 and 14. The decrease was greater than 1.0 g/dL in 8.6% and greater than 0.6 in 24.3% of the infants. Of the nonanemic infants, 22% became anemic. Serum iron and percentage saturation of transferrin decreased, whereas serum ferritin increased significantly. Mean cell volume, iron-binding capacity, protoporphyrin, and haptoglobin did not show changes. Reticulocyte index and erythropoietin increased significantly at 30 days. Leukocyte counts, Zetacrit, and C-reactive protein did not help to predict the hemoglobin decrease. These results suggest that a mild viral infection in infants induces a significant decrease in hemoglobin that may persist for 14 to 30 days and may be difficult to distinguish from iron deficiency.
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PMID:Anemia of a mild viral infection: the measles vaccine as a model. 279 79

Previous studies have indicated a high incidence of nonanemic iron deficiency in high school runners, but little is known regarding participants in other sports. The hematologic and iron status of 30 high school swimmers was assessed at the beginning and end of a competitive swim season. Iron depletion (serum ferritin level less than 12 micrograms/L) was initially present in 46.7% of the girls and none of the boys, yet among those subjects with hypoferritinemia there was no evidence of impaired red blood cell production. Serum haptoglobin levels were normal and did not correlate with serum ferritin levels. No significant change was observed in ferritin, hemoglobin, or haptoglobin concentrations during the course of the season. Dietary intake of iron was poor, particularly in the girls, in whom it averaged 43% of the recommended dietary allowance. Menstrual histories suggested an inverse relationship between the amount of menstrual flow and the serum ferritin level. These findings indicate a high prevalence of nonanemic iron deficiency in female high school swimmers that bears no relationship to swim training. Dietary inadequacies and menstrual blood flow appear to be important contributors to the hypoferritinemia observed in these athletes.
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PMID:Iron deficiency in athletes. Insights from high school swimmers. 291 91

The mechanisms for acquisition of iron by Haemophilus influenzae and their role in pathogenesis are not known. Heme and nonheme sources of iron were evaluated for their effect on growth of type b and nontypable strains of H. influenzae in an iron-restricted, defined medium. All 13 strains acquired iron from heme, hemoglobin, hemoglobin-haptoglobin, and heme-hemopexin. Among nonheme sources of protein-bound iron, growth of H. influenzae was enhanced by partially saturated human transferrin but not by lactoferrin or ferritin. Purified ferrienterochelin and ferridesferrioxamine failed to provide iron to H. influenzae, and the supernatants of H. influenzae E1a grown in iron-restricted medium failed to enhance iron-restricted growth of siderophore-dependent strains of Escherichia coli, Salmonella typhimurium, and Arthrobacter terregens. Marked alterations in the profile of outer membrane proteins of H. influenzae were observed when the level of free iron was varied between 1 microM and 1 mM. Catechols were not detected in the supernatants of strain E1a; however, iron-related hydroxamate production was detected by two biochemical assays. We conclude that the sources of iron for H. influenzae are diverse. The significance of hydroxamate production and iron-related outer membrane proteins to H. influenzae iron acquisition is not yet clear.
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PMID:Iron acquisition by Haemophilus influenzae. 296 10

As more studies are done on the iron status of athletes, the significance of apparent iron deficiency remains controversial. Do observed changes in iron status in athletes indicate an actual iron deficiency or a physiological response to exercise? Iron replacement would clearly be indicated if an iron deficiency was present but would not be necessary or effective if the observed changes were simply a physiological response. There is agreement that serum ferritin and haemoglobin decrease with some exercise conditions and that some indicators of haemolysis, such as serum haptoglobin and bilirubin, change in response to exercise. Expansion of plasma volume and the shift of iron storage from bone marrow to the liver could support the claim that the apparent reduced iron status parameters occurring with exercise are misleading. Countering this concept are studies in athletes which demonstrate dietary iron intake deficiencies and blood loss in the gastrointestinal and urinary tract. Iron deficiency is common in the general population, particularly in women. Therefore, continued monitoring of iron status in athletes appears justified in the face of present knowledge. Replacement therapy, when iron deficiency is apparent, is recommended.
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PMID:Iron status in athletes. An update. 304 28


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