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)

1. Aluminum is an established neurotoxin. Prolonged exposure to even low levels of aluminum permit its chelation and subsequent transport to brain where it is non-uniformly distributed. 2. Available evidence suggests that (i) aluminum interferes with glucose metabolism by inhibiting hexokinase and glucose-6-phosphate dehydrogenase; (ii) it binds to calmodulin and affects numerous phosphorylation-dephosphorylation reactions; (iii) it binds to transferrin and ferritin, affects the function of these proteins which in turn affect iron metabolism. 3. Thus accumulation of aluminum-induced metabolic errors colocalized in specific areas of the brain may lead to neurological disorders.
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PMID:Neurochemical hypothesis: participation by aluminum in producing critical mass of colocalized errors in brain leads to neurological disease. 167 37

174 serum ferritin assays in 121 patients with various haemolytic disorders have been performed. The mean serum ferritin levels were significantly increased in all these disorders in contrast to healthy controls. The highest serum ferritin levels were found in pyruvate kinase (PK) deficiency, moderate increase was observed in hereditary sphaerocytosis (HS) and in autoimmune haemolytic anaemia (AIHA) with massive haemolysis and in glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. Mild elevation of serum ferritin levels was depicted in paroxysmal nocturnal haemoglobinuria (PNH), in beta thalassaemia minor and in other types of haemoglobinopathies. The range of values was associated with a degree of haemolysis and its relation to duration of the disease was not apparent in most cases. Highly significant differences between serum ferritin levels in splenectomized and non-splenectomized patients with HS and between serum ferritin levels in patients with AIHA with massive haemolysis or in remission were found. As compared to normal controls, significant increase of serum ferritin levels was observed even in patients with AIHA in remission or in splenectomized patients with HS. In two patients with PK deficiency the levels exceeding 2,000 micrograms/l indicated manifest iron overload. A reliability of serum ferritin assay as an index of iron stores in haemolytic disorders has been discussed.
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PMID:Serum ferritin in patients with various haemolytic disorders. 169 23

At birth, 24 Standardbred foals were assigned at random to 1 of 2 groups and were given a placebo supplement (group 1) or an iron supplement (248 mg of iron/treatment; group 2). Foals were given iron supplement or placebo 4 times during the second and third weeks after birth. Hematologic variables and general health were monitored until foals were 4 months old. Mean PCV in foals of both groups decreased during the first 2 weeks after birth, but values remained within adult horse reference ranges. During the first 6 weeks after birth, foal erythrocytes were smaller than adult horse erythrocytes, but foal erythrocyte glucose-6-phosphate dehydrogenase activity was greater than that in adult horses. At every measurement, indices of anisocytosis were lower in foals, compared with adult horse reference values, suggesting that foals have a homogeneous population of microcytic erythrocytes during early foalhood. In 2-week-old foals of both groups and in 4-week-old placebo-treated foals, mean serum iron concentration was lower than that in adult horses. In foals at birth and during the first 4 months, total iron-binding capacity values were above the adult reference range. In newborn foals, transferrin saturation percentage values decreased to below the reference range in foals from 2 weeks to 4 months after birth. When foals were born, serum ferritin concentration values were above the adult horse reference range, but decreased to within the reference range by the time foals were 1 day old. From 2 through 6 weeks after birth, foal ferritin concentration values were below the adult reference range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microcytosis, hypoferremia, hypoferritemia, and hypertransferrinemia in standardbred foals from birth to 4 months of age. 238 18

Erythrocyte deficiency may lead to shortened erythrocyte life-span and also influence iron metabolic processes. Haemoglobin, serum iron, transferrin and ferritin concentrations and total iron-binding capacity (TIBC) were compared in 74 normal and 68 glucose-6-phosphate dehydrogenase (G6PD) deficient subjects to investigate this possibility. All the parameters were measured using standard biochemical and immunoelectrophoretic methods. Haemoglobin and serum iron concentrations were similar in both groups of subjects. It was found that G6PD deficient subjects had significantly greater transferrin (P less than 0.001), ferritin (P less than 0.001) and TIBC (P less than 0.01) values compared to normal subjects. Some possible causes of these observations are discussed.
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PMID:Haemoglobin, serum iron, transferrin, ferritin concentrations and total iron-binding capacity in erythrocyte glucose-6-phosphate dehydrogenase deficiency. 345 11

Trypanosoma brucei EATRO 110 infection in deer mice (Peromyscus maniculatus) produced anemia in 15 of 42 mice between postinoculation days 14 and 70. The infected anemic (IA) mice had significantly higher reticulocyte counts (P less than 0.025), spleen (P less than 0.001) and liver (P less than 0.005) weights, and higher parasitemia than did infected nonanemic (INA) mice. gamma-Globulin concentrations of infected mice were markedly increased, and values for INA mice were 10% higher than values for IA mice. Erythrocyte hexokinase, glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase, and pyruvate kinase activities were increased in infected mice, whereas phosphofructokinase was only slightly decreased in infected mice. Seemingly, development of anemia was not related to defects in erythrocyte metabolism. Serum iron values of infected mice were similar to those of controls. Storage iron (hemosiderin and ferritin) concentrations were increased in the spleen and to a lesser extent in the liver. The activity of superoxide dismutase, an enzyme that favors conversion of easily mobilized soluble ferritin to poorly mobilized insoluble hemosiderin, was decreased per unit weight of the enlarged spleen, although total activity was increased. The superoxide dismutase activity per unit weight of liver was not altered in infected mice although total liver activities were increased. These findings, as well as the marked reticulocytosis, indicate that lack of iron supply does not have a part in precipitating the anemia of T brucei infection. Leukocytosis was present in infected animals and was associated with lymphocytosis, eosinopenia, basophilia, and monocytosis; these changes were more marked in IA than in INA mice.
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PMID:Pathogenesis of Trypanosoma brucei infection in deer mice (Peromyscus maniculatus): hematologic, erythrocyte biochemical, and iron metabolic aspects. 686 60

Many studies have shown that oxygen radicals can be produced during arsenic metabolism. We report here that in human fibroblasts (HFW cells) sodium arsenite exposure caused increased formation of fluorescent dichlorofluorescein (DCF) by oxidation of the nonfluorescent form. The enhanced DCF fluorescence was inhibited by a radical scavenger, butylated hydroxytoluene. The effects of sodium arsenite treatment on cellular antioxidant activities were then examined. Treatment of HFW cells with sodium arsenite resulted in a significant increase in heme oxygenase activity and ferritin level. Sodium arsenite-enhanced heme oxygenase synthesis was inhibited by co-treatment of cells with the antioxidants sodium azide and dimethyl sulfoxide. Furthermore, sodium arsenite treatment did not apparently affect glucose-6-phosphate dehydrogenase activity, but resulted in significantly increased glutathione levels and superoxide dismutase activity, slightly decreased glutathione peroxidase activity, and significantly decreased catalase activity. Sodium arsenite toxicity was partly reduced by addition of catalase to the culture medium. These results imply that arsenite can enhance oxidative stress in HFW cells.
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PMID:Modulation of cellular antioxidant defense activities by sodium arsenite in human fibroblasts. 852 46

Toxicosis syndrome of fasting pregnant ewes has a close similarity to human preeclampsia (hypertension, albuminuria). The common etiological factor might be oxidative hemolysis and heme-induced endothelial damage. Ewes (5 starving, 5 control) at 130-135 gestational days with a 96-h fasting period followed by refeeding were used. Blood pressure, platelet count, electrolytes, kidney and liver function parameters, as well as plasma glucose, hemoglobin/heme, free thiol groups and Trolox equivalent antioxidant capacity, and plasma iron and ferritin levels were measured. Statistical significance was assessed using Student's t test (P < 0.05). Besides hypertension and renal disturbances, hemolysis, elevated liver enzymes and low platelet count, characteristic of human HELLP syndrome, were also present. In the first 24 h of glucose deprivation there was a significant rise in both the plasma hemoglobin/heme and indirect bilirubin concentrations. The antioxidant free thiol levels decreased significantly the next day, without any change in the total antioxidant capacity of the plasma. While the loss of calcium and magnesium levels related to the similarity to preeclampsia, reduced plasma iron concentrations referred to species differences in iron homeostasis. An oxidative stress causing hemolysis in a glucose-6-phosphate dehydrogenase-deficient animal model was proven by the loss of free thiols after glucose deprivation. The activation of the oxidative stress protein heme oxygenase was a signal of endothelial cell injury, the primary cause of pregnancy-induced hypertension.
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PMID:The pathogenetic role of heme in pregnancy-induced hypertension-like disease in ewes. 936 99

The influence of occupational exposure to mercury vapours on the activity of the red cell enzymes [glucose-6-phosphate dehydrogenase (G-6PD), acetylcholinesterase (AChE), glutathione reductase (GR) and superoxide dismutase (SOD)], as well as on peripheral blood indices [erythrocyte number (RBC), HCT, Hb, MCHC] and on serum concentrations of iron, ferritin, transferrin and total iron binding capacity (TIBC), was assessed. Studies were carried out on 46 men aged between 21 and 56 years (X = 39 +/- 10.4) exposed to mercury vapours during their work from 7 months to 32 years (= 14.7 +/- 10.8). The control group consisted of 35 healthy workers aged between 20 and 54 years (X = 33.6 +/- 9.8) not exposed to chemical nor physical agents. In both groups studied, there were 50% and 34.3% smokers, respectively. The activity of studied red cell enzymes--G-6PD, AChE, GR and SOD--was estimated according to the colorimetric methods described by Beutler and expressed as international units per gram of hemoglobin (IU g Hb(-1)). Peripheral blood cell parameters were determined using an automatic cell counter. The concentration of serum iron and TIBC was determined using colorimetric methods (Beckman), while that of ferritin and transferrin by nephelometric methods. The time-weighted average (TWA) of mercury concentration in the air determined before the study was 0.0028 mg m(-3). Statistical analysis of the data was performed using either the Cochran and Cox C-test or the Student's t-test. The medium mercury concentration in the urine was 77.44 +/- 48.15 microg l(-1). In the group exposed to mercury vapours, a significant decrease was found in G-6PD activity (23.9%, P<0.001), GR (18.8%, P<0.001), and SOD (5%, P<0.001) with a concomitant increase in AChE activity (35.9%, P<0.001) was found. Moreover, a statistically significant increase occurred in HCT and RBC, and a decrease in MCV and MCHC as well as increases of ferritin (130.9%, P<0.001), transferrin (118.4%, P<0.001) and TIBC (11.2%, P<0.05). Our results indicate that long-term exposure to mercury vapours induces changes in the activity of red cell enzymes--G-6PD, AChE, GR and SOD--and may also influence other important hematological parameters of the peripheral blood.
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PMID:The activity of erythrocyte enzymes and basic indices of peripheral blood erythrocytes from workers chronically exposed to mercury vapours. 1079 23

CDKN2A is regarded as a major melanoma susceptibility gene. A 19 bp deletion has been detected within Dutch families with familial atypical multiple mole-melanoma syndrome. Genetic analysis revealed two individuals with germline deletions in both copies of CDKN2A. One of them did not develop atypical naevi or melanoma, but died of adenocarcinoma at the age of 54 years. This report describes the results of the investigation of the second p16-null individual, who was also found to have glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and who has developed many atypical naevi and seven melanomas. Using electron microscopic techniques, striking alterations in melanosomal structures and deviations in their sulphur, iron and calcium composition indicating a strong preference for phaeomelanogenesis and increased oxidative stress were found in the naevus cells of the patient. Using an in vitro model, we demonstrated that leaking melanin precursors may strongly enhance oxidative DNA damage through iron release from ferritin. We conclude that the homozygous p16 deletion is not sufficient for the development of a dysplastic naevus phenotype and melanoma. However, when an additional modifying factor, such as G-6-PD deficiency, increases the level of oxidative DNA damage in melanin-producing cells, the risk of developing atypical naevi and their malignant transformation may increase significantly.
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PMID:Homozygous germline mutation of CDKN2A/p16 and glucose-6-phosphate dehydrogenase deficiency in a multiple melanoma case. 1269 Mar 1

The refracton hypothesis describes the lens and cornea together as a functional unit that provides the proper ocular transparent and refractive properties for the basis of normal vision. Similarities between the lens and corneal crystallins also suggest that both elements of the refracton may also contribute to the antioxidant defenses of the entire eye. The cornea is the primary physical barrier against environmental assault to the eye and functions as a dominant filter of UV radiation. It is routinely exposed to reactive oxygen species (ROS)-generating UV light and molecular O(2) making it a target vulnerable to UV-induced damage. The cornea is equipped with several defensive mechanisms to counteract the deleterious effects of UV-induced oxidative damage. These comprise both non-enzymatic elements that include proteins and low molecular weight compounds (ferritin, glutathione, NAD(P)H, ascorbate and alpha-tocopherol) as well as various enzymes (catalase, glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase, and superoxide dismutase). Several proteins accumulate in the cornea at unusually high concentrations and have been classified as corneal crystallins based on the analogy of these proteins with the abundant taxon-specific lens crystallins. In addition to performing a structural role related to ocular transparency, corneal crystallins may also contribute to the corneal antioxidant systems through a variety of mechanisms including the direct scavenging of free radicals, the production of NAD(P)H, the metabolism and/or detoxification of toxic compounds (i.e. reactive aldehydes), and the direct absorption of UV radiation. In this review, we extend the discussion of the antioxidant defenses of the cornea to include these highly expressed corneal crystallins and address their specific capacities to minimize oxidative damage.
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PMID:The role of corneal crystallins in the cellular defense mechanisms against oxidative stress. 1807 95


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