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)

Low density lipoprotein (LDL) oxidation mediated by phorbol myristate acetate (PMA)- and formylmethionylleucylphenylalanine (FMLP) -stimulated human neutrophils was enhanced by 70% in the presence of ferritin. Iron released from ferritin by the superoxide anion generated in the respiratory burst of stimulated neutrophils is shown to be involved in lipoprotein oxidation. Ascorbate (100 microM), superoxide dismutase (10 micrograms/ml) and uric acid (430 microM) showed inhibitory effects of 30% [corrected], 70% and 50% on LDL oxidation, respectively. Ceruloplasmin (2.7 microM) potentiated LDL oxidation by stimulated neutrophils and ferritin, both alone and in the presence of methionine. Methionine (1 mM) and catalase (30 micrograms/ml) increased LDL oxidation by stimulated neutrophils and ferritin. These data suggest that LDL oxidation by stimulated neutrophils and ferritin may be relevant in inflammation when both neutrophils and ferritin are increased.
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PMID:Low density lipoprotein oxidation by stimulated neutrophils and ferritin. 133 54

Inhibitory effects of soybean protein isolate (SPI) and soybean lectin on the intestinal absorption of nonheme iron were investigated by in vivo studies in rats. Rats fed the SPI-based diet absorbed significantly less iron than did control rats fed the casein-based diet. Supplementing the SPI diets with 8% D-galactose significantly increased the incorporation of iron into liver ferritin, although D-galactose did not significantly increase iron absorption. Heat treatment of SPI significantly increased iron absorption. Ascorbate did not enhance iron absorption in rats fed the SPI-based diet. The presence of lectin in an aqueous extract of SPI was suggested by hemagglutination activity as well as by immunoreactivity with soybean lectin antibody. Soybean lectin introduced into ligated segments of the upper small intestine of rats inhibited ferrous iron absorption. This inhibitory effect, especially in the mucosal uptake, was significantly improved by addition of N-acetyl-D-galactosamine to soybean lectin. Soybean lectin had no effect on ferric iron absorption. Our results suggest that a portion of the reduction in iron absorption in rats fed SPI may be due to lectins.
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PMID:Soybean protein isolate and soybean lectin inhibit iron absorption in rats. 156 73

Dietary, anthropometric, and chronic disease risk factors (CDRF) in vitamin/mineral supplement users (U) and non-users (NU) were measured in a farm population consisting of 162 subjects (46% females and 54% males; 20-79 years of age, mean age: 52 years). Subjects were white, except for two black males. Supplements were used by 62 subjects (38%); 47% of females and 31% of males used supplements; 43% of subjects over 50 years of age and 32% of subjects age 50 or under used supplements. Both dietary intake and energy expenditure were measured using 4-day records. Indices of adiposity included body weight, BMI, and estimated body fat. Total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-C), serum ferritin, hemoglobin, hematocrit, zinc, copper, and vitamin C were based on 12-hr fasting blood samples. Dietary intake (excluding supplements) for vitamin/mineral U was greater than NU for vitamin C (p = 0.006), thiamin (p = 0.01), riboflavin (p = 0.03), niacin (p = 0.02), folic acid (p = 0.001), vitamin B6 (p = 0.01), and magnesium (p = 0.019). Vitamin C levels were significantly higher and the sum of four skinfolds was significantly lower among U than NU. In this population, 24% of males and 18% of females had TC levels over 240 mg%; 8% of both males and females had blood pressures (BP) greater than 140/90 mm Hg, while 49% of males and 46% of females had BP between 120/80 and 140/90; and 71% of males were more than 25% fat, and 56% of females were more than 35% fat. Despite the high prevalence of CDRF, there were no significant differences between supplement U and NU.
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PMID:Chronic disease risk factors in vitamin/mineral supplement users and nonusers in a farm population. 189 83

Iron is essential to cell metabolism but promotes free radical damage to membranes and lipids. Therefore, excess intracellular iron is stored within the shell of hollow ferritin molecules until needed for metabolic use. Ascorbate retards ferritin degradation and increases iron bioavailability. The vitamin stabilizes the iron cores of ferritin in cells prelabeled with 59Fe. [35S]Methionine labeling demonstrates that this enhanced stability of the iron cores results from delayed degradation of the ferritin shells. Subcellular fractionation of 59Fe-labeled cells by use of a Sepharose CL-6B column shows that ascorbate significantly delays the shift of ferritin label from the cytosolic to the lysosomal compartment. Monomeric ferritin shells in the cytoplasm gradually form clusters that bind to lysosomes. Single ferritin shells do not. Ascorbate does not affect the conversion of cytoplasmic ferritin monomers to clusters but greatly retards the autophagic uptake of ferritin clusters into lysosomes.
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PMID:Ascorbic acid and iron metabolism: alterations in lysosomal function. 196 68

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

6-hydroxydopamine (6-OHDA) proved to be a very effective agent for iron release from ferritin. Iron release was enhanced in the presence of SOD, catalase and under anaerobic conditions. Ascorbic acid, a well known agent able to release iron from ferritin, increased the amount of released iron in more than an additive manner when used in combination with 6-OHDA. Similar to 6-OHDA, 6-hydroxydopa (Topa) and 1,2,4-benzenetriol were also able to release iron in large amounts; in contrast, catecholamines and other benzenediols were comparatively ineffective.
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PMID:Release of iron from ferritin by 6-hydroxydopamine under aerobic and anaerobic conditions. 212 9

We investigated response sensitivities of indices of iron status to controlled iron depletion and repletion in 11 premenopausal women. The women were depleted of storage iron (as reflected by serum ferritin) through a combination of a low-iron diet and phlebotomy. They then consumed a diet containing 13.7 mg of iron per 2000 kcal, supplemented with either ascorbic acid or placebo (for 5 1/2 weeks) and a daily 50-mg iron supplement (for the subsequent 17 days). The relative sensitivities of different indices for detecting iron depletion were as follows: ferritin greater than % transferrin saturation greater than plasma iron greater than hemoglobin greater than hematocrit greater than zinc protoporphyrin (ZnPP) and erythrocyte protoporphyrin (EP). Ascorbic acid treatment during repletion, before iron supplementation, significantly (P less than 0.05) affected changes in hemoglobin, ZnPP, ZnPP/heme, and EP/heme. Changes in heme synthesis evidently do not occur until iron stores are depleted and, conversely, during iron repletion hematopoiesis must be satisfied before iron stores, as reflected by ferritin, increase. Thus, the use of only one index of iron status is of limited value for detecting iron depletion.
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PMID:Response of various indices of iron status to acute iron depletion produced in menstruating women by low iron intake and phlebotomy. 231 Dec 19

Pretreatment of cultured hepatocytes with the ferric iron chelator deferoxamine prevents the killing of the cells by tert-butyl hydroperoxide (TBHP). Incubation of the deferoxamine-pretreated hepatocytes in a serum-free medium containing only 0.25 nM iron restored the sensitivity of the cells to TBHP within 4 to 6 hr. An amino acid-free medium accelerated the restoration of sensitivity in parallel with an enhanced rate of degradation of 14C-prelabeled protein. By contrast, inhibitors of the autophagic degradation of protein, including chymostatin, 3-methyladenine, benzyl alcohol, colchicine, oligomycin, and methylamine, inhibited the restoration of sensitivity of deferoxamine-treated hepatocytes to TBHP in parallel with their inhibition of protein degradation. With chymostatin, 3-methyladenine, benzyl alcohol, and colchicine, there was a parallel dose dependency of both the inhibition of protein turnover and the inhibition of the restoration of sensitivity to TBHP. Ascorbic acid, known to specifically retard the autophagic degradation of ferritin, inhibited the restoration of sensitivity to TBHP without effect on the general rate of protein turnover. None of the agents studied had any protective effect on the toxicity of TBHP for hepatocytes that were not pretreated with deferoxamine. These data indicate that the autophagic degradation of protein generates a pool of ferric iron required for the killing of cultured hepatocytes by TBHP.
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PMID:Autophagic degradation of protein generates a pool of ferric iron required for the killing of cultured hepatocytes by an oxidative stress. 231 91

The effect of ascorbic acid on iron retention from a diet with predicted low iron bioavailability (containing minimal meat and ascorbic acid) was investigated in iron-depleted premenopausal women. Eleven women were depleted of storage iron (indicated by serum ferritin) through a combination of diet (5.0 mg Fe/2000 kcal for 67-88 d) and phlebotomy. They then consumed a diet containing 13.7 mg Fe/2000 kcal, supplemented with placebo or ascorbic acid three times daily (1500 mg total) with meals for 5.5 wk. Ascorbic acid improved apparent iron absorption (balance method) [38 +/- 2% (means +/- SEM) vs 27 +/- 2%]. Ascorbic acid also improved hemoglobin, erythrocyte protoporphyrins, and serum iron but not hematocrit, serum ferritin, iron-binding capacity, or transferrin saturation. In iron-depleted women consuming a diet with predicted poor iron availability, ascorbic acid supplementation enhanced body iron retention for 5.5 wk.
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PMID:Ascorbic acid: effect on ongoing iron absorption and status in iron-depleted young women. 232 71

Ascorbic acid blocks the degradation of cytoplasmic ferritin by reducing lysosomal autophagy of the protein.
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PMID:Ascorbic acid and ferritin catabolism. 266 91


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