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)

Three experiments involving 52 baby pigs were conducted to determine the minimum copper requirement of baby pigs fed purified diets. Diets were supplemented with anhydrous cupric sulfate to yield the following copper concentrations (ppm, by analysis) when the three experiments were combined: 0.6, 0.9, 1.3, 1.9, 2.0, 2.8, 3.2, 4.0, 4.9, 5.6 and 9.3. Parameters examined include weight gain, hematocrit, hemoglobin concentration, mean corpuscular hemoglobin concentration, plasma ceruloplasmin activity, plasma copper concentration, copper balance, brain and erythrocyte superoxide dismutase activity, copper concentration of liver, kidney, spleen, heart, brain, femur and hair, liver ferritin-iron and total iron concentration, strength characteristics of the femur, and gross and histological appearance at necropsy. Weight gains were subnormal at dietary copper concentrations below 1.9 ppm; plasma ceruloplasmin activities, and plasma and tissue copper concentrations were depressed at dietary copper levels below 2.8 ppm. Bone histopathology was evident at dietary copper levels below 3.2 ppm, and copper balance was low at dietary copper levels below 4.9 ppm. Some evidence of anemia was present at dietary copper levels below 5.6 ppm. Under the conditions of this study, the copper requirement of the baby pig fed a purified diet was judged to be approximately 5.6 ppm (6 ppm copper, dry basis).
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PMID:Copper requirement of baby pigs fed purified diets. 44 53

Factors related to iron metabolism were determined in 20 United States Navy divers during 8 d of air saturation-excursion hyperbaric exposures. During these simulated dives progressive and correlated increases in serum ferritin and iron occurred. No significant changes were observed in bilirubin, hemoglobin, ceruloplasmin, transferrin, copper, or total iron binding capacity. The significance of the increased serum ferritin is discussed in relation to bone marrow damage and early detection of aseptic bone necrosis.
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PMID:Changes in serum ferritin and other factors associated with iron metabolism during chronic hyperbaric exposure. 45 20

Sheep were treated with large amounts of copper (20 mg of CuSO4,5H2O/kg body wt. per day) for 9 weeks to examine the effect of copper excess on iron metabolism. In addition to confirming that massive haemolysis and accumulation of copper occurs in the liver, kidney and plasma after 7 weeks of exposure to excess copper, it was observed that excess copper produced an increased plasma iron concentration and transferrin saturation within 1 week. Further, iron preferentially accumulated in the spleen between 4 and 6 weeks of copper treatment, producing 3-fold increases in the iron content of both the ferritin and non-ferritin fractions. A 3-4 fold increase was also observed in the amount of ferritin that could be isolated from the spleen. The copper treatment had little or no effect on the concentration of iron in the liver and bone marrow. The following properties of erythrocytes were also unaffected by copper treatment: size, haemoglobin content and pyruvate kinase activity, although the erythrocyte concentration of copper increased after 6 weeks. Copper accumulated in the spleen between 6 and 9 weeks, probably owing to the phagocytosis of erythrocytes containing high concentrations of copper. The data suggest that copper excess influences iron metabolism, initially by causing a compensated haemolytic anaemia, and later by interfering with re-utilization of iron from ferritin in the reticuloendothelial cells of the spleen.
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PMID:The effect of copper excess on iron metabolism in sheep. 62 72

Much can be gained by reassessing the processes which determine the ability of lysosomes to take up or exclude, sequester and mobilize heavy metals. To achieve a better understanding of these events, the chemical forms, intracellular pathways and modes of delivery of metals to lysosomes, as well as the specific physiologic ligands and molecular targets susceptible to metal toxicity have to be identified. None of these can be derived from measurements of metal contents of whole lysosomal fractions because the metal's "effective concentration" at a specific target site may be affected by the binding properties of the lysosomal ligand as well as by those of cation carrier proteins present in the cytosol (e.g., metallothionein), and by interactions with and competitions by other cellular organelles. Therefore, the possibility of such events diminishing or enhancing a metal's direct effect observable in in vitro systems has to be considered before extrapolating to the in vivo situation. Another pitfall to be wary of is the equation of an organelle's relative affinity for a metal in vitro with its susceptibility to the metal's toxic effects. This is evident, albeit at a tissue level rather than at that of organelles, from the discordance between the low affinity of nervous tissue for lead and this metal's pronounced encephalopathic effect. The answers to some of the questions raised in this review may possibly lead to pharmacologic applications, particularly to the development of effective agents for the removal from or the inactivation of toxic metals deposited in lysosomes. At present, considerable uncertainty exists regarding the possible interaction of therapeutic chelating agents with lysosomes in vivo. We do not know, for example, whether the contrasts between the remarkable effectiveness of penicillamine in mobilizing copper from tissues and the limited effectiveness of desferioxamine in removing excess iron stores can be accounted for by differences in accessibility of these two chelators to lysosomes. Or, alternatively, can these differences in effectiveness be related to different ligands or macromolecules interacting with each metal? At least part of the lysosomal iron is bound to ferritin molecules which may not be susceptible to the action of chelating agents after incorporation. Such speculation is not without foundation since ferritin molecules are heterogeneous. However, whether this heterogeneity, which is reflected in different organ-specific patterns of distribution (Powell et al. 1973), is the result of differing affinities of the isoferritins for specific subcellular organelles has not been established. It is conceivable that ferritin molecules present in the cytoplasm may be subtly different from those taken up by lysosomes, implying that the latter are endowed with capabilities for selection of specific macromolecules...
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PMID:Heavy metals and lysosomes. 78 27

The effect of long-term dietary cadmium treatment upon the distribution of the metals copper, iron and zinc has been compared in various organs of male and female rats. The renal accumulation of cadmium was similar in both sexes without a plateau being reached. In contrast, the hepatic accumulation of cadmium was higher in the female than in the male rat and a plateau was observed after 30-35 weeks of dietary cadmium treatment. Most of the cadmium which accumulated in these organs was recovered in the metallothionein fraction andthe concentration of hepatic cadmiumthionein in the female rat was correspondingly higher than in the male rat. Accumulation of cadmium was associated with an increased zinc concentration in the liver and an increased copper concentration in the kidney; these increases were correlated with increases in liver and kidney metallothioneins induced by cadmium. Uptake of cadmium into organs other than liver and kidney occurred to a small extent but was not associated with changes in the concentration of copper and zinc. Cadmium also accumulated in the intestinal mucosa where it could be recovered in a fraction corresponding to metallothionien. A loss of iron from the liver and kidney was also observed following dietary cadmium treatment and involved mainly a loss of iron from ferritin.
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PMID:Influence of dietary cadmium on the distribution of the essential metals copper, zinc and iron in tissues of the rat. 100 32

The present study was conducted to evaluate the effects of fibre supplementation on zinc, iron and copper status in human subjects. Ten males (53 +/- 8 years of age) participated in this study which consisted of three phases: baseline-1 period (2 weeks) in which subjects were on their normal, habitual dietary intake, followed by a period of fibre supplementation (5 weeks) in which subjects were supplemented with 26 g dietary fibre/d, and baseline-2 period (4 weeks) in which fibre supplement was withdrawn. Parametric measurements of zinc, iron and copper status were conducted on weeks 1,2 (zero-time), 7 and 11. Results showed that fibre supplementation for 5 weeks did not cause any significant change in the status of zinc (measured by concentration of zinc in plasma and urine and alkaline phosphatase activity), iron (measured by packed cell volume (PCV%), HB, transferrin saturation % and ferritin), or copper (measured by plasma copper concentration and erythrocyte superoxide dismutase activity). We conclude that consumption of sugar-beet fibre added to the daily diet does not constitute any risk with respect to zinc, iron and copper nutriture.
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PMID:The effects of sugar-beet fibre supplementation for five weeks on zinc, iron and copper status in human subjects. 131 63

Plasma zinc, copper, selenium, ferritin and whole blood manganese concentrations were measured in 22 children with kwashiorkor on admission to hospital and on days 5, 10 and 30 of refeeding. Twenty similarly aged, healthy, well nourished children served as controls. The mean (SEM) zinc, copper and selenium concentrations of 7.5 (0.93), 10.8 (0.64) and 0.29 (0.02) mumol/l, respectively, in the children with kwashiorkor on admission were all significantly lower than the values of 13.7 (0.66), 25.6 (1.72) and 0.72 (0.04) mumol/l in the controls. In contrast, the erythrocyte manganese level of 1.67 (0.09) micrograms/gHb and the median ferritin concentration of 293 micrograms/dl were significantly higher than in the controls. After 30 days there was full clinical recovery with significant weight gain and a return of the plasma albumin, caeruloplasmin, copper and ferritin to normal. However, manganese remained elevated and zinc and selenium concentrations remained significantly low. Our results suggest that nutritional rehabilitation of children with kwashiorkor is incomplete by 30 days and cannot be judged purely by a return of the plasma proteins to normal. Addition of selected trace elements to the diet may hasten full recovery.
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PMID:Plasma zinc, copper, selenium, ferritin and whole blood manganese concentrations in children with kwashiorkor in the acute stage and during refeeding. 137 81

This study examined the effect of diet-induced, marginal zinc deficiency for 7 wks in 15 men (aged 25.3 +/- 3.3 yrs; mean +/- SD) on selected indices of iron and copper status. The regimen involved low-zinc diets based on egg albumin and soy protein with added phytate and calcium such that mean [phytate]/[Zn] and [phytate] X [Ca]/[Zn] molar ratios were 209 and 4116, respectively, for 1 wk, followed by 70 and 2000, respectively, for 6 wks. Subjects were then repleted with 30 mg Zn/d for 2 wks. Plasma copper, Cu,Zn-superoxide dismutase (Cu,Zn-SOD) activity in plasma and red blood cells (RBC), hemoglobin, hematocrit, and serum ferritin were determined weekly on fasting blood samples. Significant reductions (p less than 0.05) after 7 wks in RBC Cu,Zn-superoxide dismutase (49.5 +/- 7.2 vs 33.6 +/- 6.3 U/mg Hb) and serum ferritin (69.2 +/- 38.7 vs 53.8 +/- 33.7 micrograms/L) occurred; no comparable decline was noted for plasma Cu, hemoglobin, or hematocrit. Significant (p less than 0.05) but less consistent changes were also observed in plasma superoxide dismutase activity. None of the changes were associated with the decreases in plasma, urinary and hair zinc concentrations, and alkaline phosphatase activity in RBC membranes. Results indicate that the biochemical iron and copper status of the subjects was marginally impaired, probably from the dietary regimen that induced marginal zinc deficiency.
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PMID:Indices of iron and copper status during experimentally induced, marginal zinc deficiency in humans. 138 39

A 55-year-old female with progressed dementia, cerebellar ataxia was reported. There was no family history of the same symptoms although her brothers, sisters and a son showed hypoceruloplasminemia and decrease of the serum copper content. On physical examination, anemia, dementia, dysarthria, torticollis, choreic involuntary movement of respiratory muscles, hyperreflexia in extremities and cerebellar ataxia were noted. Blood analysis revealed microcytic hypochromic anemia, diabetes mellitus, decrease of copper content of the serum and urine. Serum ferritin concentration was increased. Serum ceruloplasmin could not be detected. Biopsy of the liver showed that copper content in the liver was slightly increased and iron content was remarkably increased. On MRI study, dentate nucleus of the cerebellum, the thalamus, the putamen and the caudate nucleus and the liver showed low intensity in both T1 and T2 weighted images. Based on increased iron content in the liver, the radiological findings of the brain suggested deposition of iron in the brain. This deposition was considered as caused by deficiency of function of ceruloplasmin as ferroxidase. This disorder is suggested as a new disease due to ceruloplasmin deficiency different from Wilson's disease.
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PMID:[A case of ceruloplasmin deficiency which showed dementia, ataxia and iron deposition in the brain]. 145 25

Superoxide and hydrogen peroxide are reactive oxygen species (ROS) primarily produced by phagocytic cells as a consequence of the process of phagocytosis. This defensive role, may, however, become one of attack when production of ROS is excessive and overwhelms cellular scavenging systems. This happens in situations such as acute inflammation and results in host cell membrane damage, which is particularly prevalent in the presence of transition metal catalysts such as iron and copper. The skin is uniquely vulnerable to this attack being rich in polyunsaturated fatty acids and exposed to high oxygen tensions and ultraviolet light, both of which promote production of ROS. Additionally, the respiratory burst of infiltrating polymorphonuclear leukocytes and macrophages in inflamed skin will produce high local levels of superoxide that can release "catalytic iron" from storage proteins such as ferritin. The role of iron and ROS in the pathogenesis of inflammatory skin disease is discussed as is the possibility of novel therapeutic strategies based on their removal.
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PMID:Skin inflammation: reactive oxygen species and the role of iron. 146 83


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