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 examined time-dependent changes in antioxidant vitamins and oxidative damage to DNA and lipids in the bone marrow, liver, and plasma of rats given total body irradiation (TBI) with X-rays at 3 Gy. The oxidative damage to DNA and lipids was evaluated by measuring increases of 8-hydroxydeoxyguanosine (8OHdG) in DNA and 4-hydroxy-2-nonenal (HNE), respectively. After the TBI, marked increases in 8OHdG and HNE were detected at 3 to 5 h in the bone marrow, while gradual increases in these parameters were detected after a few days in the liver. These changes in 8OHdG and HNE were well correlated within each tissue. In the bone marrow, levels of both vitamin C and vitamin E were decreased by the TBI; however, the changes in vitamin C were earlier and greater than those in vitamin E. In the liver, the level of vitamin C did not decrease, but that of vitamin E decreased due to the TBI. Changes in HNE, vitamin C, and vitamin E in the plasma were similar to those in the liver. Within each tissue, the time of decrease in antioxidants was almost the same as that of the increase in oxidative damage. An increase in total iron due to the TBI was also detected in these tissues. In particular, the total iron in the bone marrow was markedly increased at a few hours after the TBI, with a slight increase in transferrin and no increase in ferritin. Exposure studies performed on cells or isolated DNA showed that an increase in 8OHdG was detected immediately after irradiation at more than 100 Gy in bone marrow cells and at less than 10 Gy in isolated DNA, suggesting that an increase in 8OHdG is undetectable even in bone marrow immediately after the TBI at 3 Gy. These results indicate that the onset of oxidative damage to DNA and lipids was delayed after TBI at 3 Gy, that it was quite different in the bone marrow and the liver, and that an increase in iron and decrease in antioxidant vitamins were involved in the mechanism of oxidative damage.
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PMID:Different onsets of oxidative damage to DNA and lipids in bone marrow and liver in rats given total body irradiation. 1167 39

Iron overload could promote the generation of free radicals and result in deleterious cellular damages. A physiological increase of oxidative stress has been observed in pregnancy. A routine iron supplement, especially a combined iron and vitamin C supplementation, without biological justifications (low hemoglobin [Hb] and iron stores) could therefore aggravate this oxidative risk. We investigated the effect of a daily combined iron supplementation (100 mg/d as fumarate) and vitamin C (500 mg/d as ascorbate) for the third trimester of pregnancy on lipid peroxidation (plasma TBARS), antioxidant micronutriments (Zn, Se, retinol, vitamin E, (beta-carotene) and antioxidant metalloenzymes (RBC Cu-Zn SOD and Se-GPX). The iron-supplemented group (n = 27) was compared to a control group (n = 27), age and number of pregnancies matched. At delivery, all the women exhibited normal Hb and ferritin values. In the supplemented group, plasma iron level was higher than in the control group (26.90 +/- 5.52 mmol/L) and TBARs plasma levels were significantly enhanced (p < 0.05) (3.62 +/- 0.36 vs 3.01 +/- 0.37 mmol/L). No significant changes were observed in plasma trace elements and red blood cell antioxidant metalloenzymes. Furthermore, the alpha-tocopherol plasma level was lowered in the iron-supplemented groups, suggesting an increased utilization of vitamin E. These data show that pharmalogical doses of iron, associated with high vitamin C intakes, can result in uncontrolled lipid peroxidation. This is predictive of adverse effects for the mother and the fetus. This study illustrates the potential harmful effects of iron supplementation when prescribed only on the assumption of anemia and not on the bases of biological criteria.
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PMID:Increased lipid peroxidation in pregnant women after iron and vitamin C supplementation. 1176 27

Based on a cross-sectional study conducted among 100 adults in 1993 in Tanga, Tanzania, the relationship between Wuchereria bancrofti infection and markers of iron, vitamin A and vitamin E status was assessed. Potential predictors assessed were elephantiasis, hydrocoele, W. bancrofti microfilaria intensity and antigen concentration, and intensity of Schistosoma haematobium, hookworm, Trichuris trichiura and Ascaris lumbricoides infection, while controlling for age, sex and elevated serum alpha-1 antichymotrypsin. Of the 100 adults, 62 had W. bancrofti antigenaemia and 43 microfilaraemia, and 21 had elephantiasis. Of the 64 males, 31 had hydrocoele. W. bancrofti microfilaria intensity was a positive predictor of serum ferritin and a negative predictor of serum alpha-tocopherol. In contrast, negative relationships observed between W. bancrofti microfilaria intensity and serum beta-carotene and retinol were not significant. Neither antigen concentration nor clinical manifestations were predictors of micronutrient status. Intensity of hookworm infection was associated with lower serum ferritin. S. haematobium egg output was not a significant predictor of serum ferritin, but was a positive predictor of serum beta-carotene. In conclusion, W. bancrofti microfilaria intensity was associated with higher serum ferritin, but lower serum alpha-tocopherol. The associations probably reflect increased oxidative stress due to microfilariaehost interactions, which could play a role in the pathogenesis.
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PMID:Serum ferritin, alpha-tocopherol, beta-carotene and retinol levels in lymphatic filariasis. 1205 4

Cellular oxidative stress is due to the production of reactive oxygen species (ROS), on the one hand, and weaknesses of the antioxidative defence, on the other. This is particularly true for cells with an active metabolism such as neurons and muscle cells, but it is also relevant for all other cell types. Hydrogen peroxide is an important member of ROS and is generated predominantly by mitochondria. In combination with reduced trace metals such as iron or copper, hydrogen peroxide is transformed into the highly reactive hydroxyl radical which causes damage to virtually all macromolecules. Oxidation of nucleic acids results in mutations while protein denaturation leads to enzyme defects and impairment of the cytoskeleton. Lipid peroxidation in cell membranes is strongly involved in the perturbation of ion homeostasis. Because this cell damage ultimatively causes cell death, oxidative stress initiates several diseases. Mitochondria play a major role in this context because they are the main source of endogenous oxidative stress and additionally function as an inducer of programmed cell death (apoptosis). Several strategies of antioxidative defence exist: While transition metals can be inactivated by chelating proteins (e.g., ferritin), ROS can be reduced enzymatically (e.g., by the glutathione peroxidase) or non-enzymatically by antioxidants (e.g., by vitamin E, vitamin C and glutathione). Stress proteins are implicated in the repair and transport of denatured proteins as well as in the inhibition of apoptosis.
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PMID:[Oxidative stress, age-dependent [correction of age-related] cell damage and antioxidative mechanisms]. 1208 May 77

The aim of our studies included measurement of serum Zn level in CAPD patients with the subsequent evaluation of relations between serum Zn and markers of nutrition, dietary intake, markers of acute phase reaction, CAPD adequacy, nitrogen balance as well as routine clinical and laboratory data. The study was performed in 81 patients treated with CAPD for up to 3 years (12 3-month study periods). Mean serum Zn concentration was 12.2 +/- 1.8 mumol/l and was decreased in 16% of patients. Positive correlation was shown between serum Zn level and prealbumin, iron, transferrin saturation, haemoglobin, mean corpuscular haemoglobin concentration and dialysis duration. Negative correlation was shown between serum Zn level and patients age as well as daily influent and effluent volumes, what means that patients in age over 65 years and those using daily inflow or outflow dialysate volume greater than 12.7 and 12.9 I, respectively, are at risk of Zn deficiency. Dietary Zn intake (9.9 +/- 2.5 mg/day) was in 96% of patients lower than that recommended for CAPD patients. Relation between Zn intake and ferritin, total cholesterol and vitamin E in serum as well as HDL-/total cholesterol ratio was shown. Our results indicate that approx. 16% of CAPD patients need Zn supplementation. Serum Zn level in CAPD patients shows a beneficial effect on serum markers of iron metabolism, blood morphology indices, serum lipid profile and increased serum vitamin E level.
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PMID:[Serum zinc concentration with reference to other markers of continuous ambulatory peritoneal dialysis patients status]. 1208 89

The present study was designed to test the biocompatibility of a new vitamin E-modified multilayer membrane compared with highly biocompatible polysulphone dialyzer and acrylonitrile dialyzer. Thirty patients (mean age 53.2 +/- 15.3 SD years; dialytic age 36 +/- 5.6 months) were selected for the study. The study was divided into three periods of 6 months (phases A, B and C). In the first phase (from Jan. 1999 to June 1999) patients undergoing maintenance bicarbonate dialysis were randomly divided into three filter groups composed, respectively, of 10 patients: acrylonitrile group, polysulphone group and vitamin E-coated dialyzer group. In the phase B (from July 1999 to Dec. 1999) and in the phase C (from Jan. 2000 to June 2000), all three groups changed their own dialysis membranes. Vitamin E-coated dialyzer causes significant decreases in beta(2)-microglobulin, ferritin and immunoglobulin G, a normalization of complement C3 and an increase of plasmatic vitamin E compared to other filters. In the VE group homocysteine decreases but not in a significant manner. In addition, this dialyzer seems not to influence lipid pattern and protein-energy malnutrition parameters. These results clearly show a positive effect of this new filter in influencing different biochemical parameters, perhaps saving vitamin E and reducing polymorphonuclear cell activation.
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PMID:Is the bioreactivity of vitamin-E-modified dialyzer an expression of increased plasmatic vitamin E concentration? 1221 39

Anaemia in pregnancy is a major public health problem in China. Anaemia in pregnant women may be related to dietary intake of nutrients. To examine the relationship between iron status and dietary nutrients, a cross-sectional study in pregnant women was carried out. The intake of foods and food ingredients were surveyed by using 24-h dietary recall. Blood haemoglobin, haematocrit, serum iron, serum ferritin, transferrin and soluble transferrin receptor were measured in 1189 clinically normal pregnant women in the third trimester of pregnancy. The results showed that the average daily intake of rice and wheat was 504.2 g in the anaemia group and 468.6 g in the normal group. Carbohydrates accounted for 63.69% and 63.09% of energy in the anaemia and normal groups, respectively. Intake of fat was very low; 18.38% of energy in anaemia group and 19.23% of energy in normal group. Soybean intake was 109.4 g/day and 63.6 g/day in the anaemia and normal groups, respectively (P < 0.001). There were lower intakes of green vegetables (172.1 g/day) and fruits (154.9 g/day) in the anaemia group than in the normal group (246.2 g/day green vegetables (P < 0.001) and 196.4 g/day fruit (P < 0.001)). Intakes of retinol and ascorbic acid were much lower in the anaemia than in the normal group (P < 0.001). In the anaemia group, vitamin A intake was only 54.76% of the Chinese recommended daily allowance (RDA) and ascorbic acid intake was 53.35% of the Chinese RDA. Intake of total vitamin E was 14.55 mg/day in the anaemia group compared with 17.35 mg/day in the normal group (P < 0.016). Moreover, intake of iron in pregnant women with anaemia was slightly lower than that in the normal group. Comparison of iron status between the anaemia and normal groups found serum iron in women with anaemia at 0.89 microg/L, which was significantly lower than 1.09 microg/L in the normal group (P < 0.001). There were lower average values of ferritin (14.70) microg/L) and transferrin (3.34 g/L) in the anaemia group than in the normal group (20.40 microg/L ferritin (P < 0.001) and 3.44 g/L transferrin (P < 0.001)). Soluble transferrin receptor was significantly higher (32.90 nmol/L) in the anaemia than in the normal group (23.58 nmol/L; P < 0.001). The results of this study indicate that anaemia might be attributed to a low iron intake, a low intake of enhancers of iron absorption and a high intake of inhibitors of iron absorption from a traditional Chinese diet rich in grains.
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PMID:Iron status and dietary intake of Chinese pregnant women with anaemia in the third trimester. 1223 Feb 29

Maternal malnutrition continues to be a major contributor to adverse reproductive outcomes in developing countries, despite longstanding efforts to fortify foods or to distribute medicinal supplements to pregnant women. The objective of this study was to test the effect of a micronutrient-fortified beverage containing 11 micronutrients (iron, iodine, zinc, vitamin A, vitamin C, niacin, riboflavin, folate, vitamin B-12, vitamin B-6 and vitamin E) on the hemoglobin, iron and vitamin A status of pregnant women in Tanzania. A group of 259 pregnant women with gestational ages of 8 to 34 wk were enrolled in a randomized double-blind controlled trial in which study women received 8 wk of supplementation. Hemoglobin, ferritin and dried blood spot retinol were measured at baseline and at the end of the supplementation period. The supplement resulted in a 4.16 g/L increase in hemoglobin concentration and a 3 micro g/L increase in ferritin and reduced the risk of anemia and iron deficiency anemia by 51 and 56%, respectively. The risk of iron deficiency was reduced by 70% among those who had iron deficiency at baseline and by 92% among those who had adequate stores. The micronutrient-fortified beverage may be a useful and convenient preventative measure, one that could help improve the nutritional status of women both before and during pregnancy and thereby help avoid some of the potential maternal and fetal consequences of micronutrient deficiencies.
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PMID:A micronutrient-fortified beverage prevents iron deficiency, reduces anemia and improves the hemoglobin concentration of pregnant Tanzanian women. 1273 Apr 20

Vitamin E supplementation could elevate circulating vitamin E metabolites while modulating oxidative and inflammatory status in end-stage renal failure patients undergoing hemodialysis. Plasma concentrations of carboxyethyl-hydroxychromanols (alpha- and gamma-CEHC), ascorbic acid, alpha- and gamma-tocopherols, F2-isoprostanes, and inflammatory biomarkers [tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), ferritin, and C-reactive protein (CRP)] were measured in blood samples obtained from patients (n = 11) before and after dialysis on two occasions prior to, and at 1 and 2 mon of daily vitamin E supplementation (400 IU RRR-alpha-tocopherol). Supplementation nearly doubled plasma alpha-tocopherol concentrations (from 18 +/- 0.5 to 31 +/- 1.7 microM, P < 0.0001), whereas gamma-tocopherol concentrations decreased (from 2.8 +/- 0.3 to 1.7 +/- 0.2 microM, P = 0.001). Serum alpha-CEHC increased 10-fold from 68 +/- 3 to 771 +/- 175 nM (P < 0.0001), and gamma-CEHC increased from 837 +/- 164 to 1136 +/- 230 nM (P = 0.008). Vitamin E supplementation also increased postdialysis hematocrits from 38 +/- 1% to 41 +/- 1% (P < 0.001). Dietary antioxidant intakes (vitamins E and C) were low in most subjects; plasma ascorbic acid levels (88 +/- 27 microM) decreased significantly with dialysis (33 +/- 11 microM, P = 0.01). Plasma IL-6, CRP, TNF-alpha, and free F2-isoprostane concentrations were elevated throughout the study. There is a complex relationship between chronic inflammation and oxidative stress that is not mitigated by short-term vitamin E supplementation. Importantly, serum vitamin E metabolite concentrations that increased 10-fold within 30 d of supplementation did not increase further, suggesting routes other than urine for removal of metabolites.
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PMID:Vitamin E supplementation increases circulating vitamin E metabolites tenfold in end-stage renal disease patients. 1457 59

A double-blind, crossover, placebo-controlled study of the effect of vitamin E on platelet functions was performed on nine splenectomized and 16 non-splenectomized beta-thalassaemia/haemoglobin E (beta-thalassaemia/HbE) patients. The patients were supplemented with a daily dose of vitamin E (525 IU) for 3 months. The functions of platelets were assessed by adenosine diphosphate (ADP)-induced platelet aggregation and adenosine triphosphate release. Plasma alpha-tocopherol, plasma thiobarbituric reactive substances (TBARs) and serum ferritin levels represented patients' antioxidant status, lipid peroxidation status and iron status respectively. Before experimentation, all patients had low plasma alpha-tocopherol levels. The splenectomized patients showed severe iron overload iron, had higher plasma TBAR levels and their platelets were more reactive to ADP than those of non-splenectomized patients. Three months of daily vitamin E supplementation resulted in a significant increase in plasma alpha-tocopherol levels and reduction in plasma TBAR levels in all patients. Serum ferritin levels of the patients were not altered; however, vitamin E reduced the platelet reactivity of the splenectomized patients towards normal levels. The influence of vitamin E on platelet reactivity may result in delaying hypoxaemia and pulmonary occlusion that commonly occurs in splenectomized beta-thalassaemia/HbE patients.
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PMID:The effects of vitamin E on platelet activity in beta-thalassaemia patients. 1461 80


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