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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the study was a more thorough assessment of the nutrition state of patients admitted to hospitals in Poland. The study was carried out in four hospitals at teaching centre level, in four hospitals at province level, and in four county hospitals. The patients for the study were selected randomly from 3310 adult patients (every 10th patient admitted to these hospitals). For the study 210 patients (122 women and 88 men) were qualified. Their mean age was 54 +/- 16 years (range 15-82 years). The patients were subjected to various biochemical tests including determination of antioxidant vitamins (vitamins A, E and C), vitamin B12, folic acid, ferritin, and homocysteine and blood lipids. Vitamin deficiency accepted as vitamin malnutrition was found in the case of vitamin C in 51.8% of the patients, folic acid in 32%, vitamin E in 10%, vitamin B12 in 6.8%, vitamin A in 1.4%. Vitamin deficiency was equally frequent in patients with malnutrition, overweight or with obesity. Lipid profile disturbances were found in 51% and high homocysteine level in 63% of the studied patients.
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PMID:[Nutritional status of patients in hospitals in Poland. More thorough assessment of nutritional status of adult patients]. 1464 80

In this study, the effects of chronically administered aluminum on iron metabolism-related parameters of liver and blood of mice were investigated. An additional purpose to determine how chronic aluminum administration together with vitamin E as an antioxidant to mice changed the parameters related to iron metabolism. For these purposes, we used 21 adult female Balb-c mice in this study. The animals were divided into three groups: one group with aluminum administered chronically, another group with aluminum plus vitamin E administered chronically, and the control group. Serum levels of hemoglobin, ferritin, iron, transferrin, hematocrit, total iron binding capacity (TIBC), as well as percentage of transferrin saturation were determined in all groups. In addition, the liver tissue levels of ferritin and iron were analyzed. Hemoglobin and hematocrit levels of the aluminum group and aluminum plus vitamin E group were significantly decreased compared to the control. In conclusion, no changes occurred in the serum iron related parameters although Al induced anemia in mice when Al administered chronically. There was an increase in the levels of liver iron and ferritin with Al, but Vit E had no effect on the changes of all blood and liver parameters caused by Al.
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PMID:Effects of chronic aluminum administration on blood and liver iron-related parameters in mice. 1500 80

Biological aging is associated with increased cellular levels of reactive oxygen species (ROS) as well as the formation and accumulation of oxidized biomolecules. During evolution, organisms developed a highly-efficient and adaptive antioxidant defense system. Antioxidants can generally be divided into two categories: enzymatic and non-enzymatic. During the aging process the activity of antioxidant enzymes, e.g. SOD, CAT, GSH-Px, and GSSG-R, depends on factors such as race, gender, tissue and subcellular localization of enzymes. The age-dependent decrease in antioxidant enzyme activity may be attributed to oxidative modifications of enzymes. During the aging process, ROS may also lead to the induction of some enzyme activity which is explained as an adaptive phenomenon. The decrease in GSH concentration with age can be explained by decreased GSH synthesis and/or increased GSH consumption in the removal of peroxides and xenobiotics. In plasma albumin, ferritin, transferrin, and caeruloplasmin exert protective action. Plasma proteins can inhibit ROS generation and lipid peroxidation by chelating free transition metals. Plasma protein concentrations changes with age. The major exogenous antioxidants, mostly derived from the diet, are vitamin E, C, A, and beta-carotene. During the aging process the level of vitamins may decrease or increase, depending on such factors as diet, and diseases.
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PMID:[Antioxidative abilities during aging]. 1507 54

In recent years, there has been an escalation in alcohol abuse and inevitably, alcohol related disorders are becoming an increasingly important cause of morbidity and mortality. Alcohol is known to induce a dose dependent increase in lipid peroxidation. Alcohol related disabilities are more pronounced when taken along with diet rich in polyunsaturated fatty acid (PUFA). The present work aims at analysing the protective role of ferulic acid (FA), a naturally occurring nutritional component on alcohol and PUFA induced oxidative stress. Two different doses of ferulic acid, 20 mg/kg body weight and 40 mg /kg body weight were used for the study. The results showed that the levels of oxidative markers; thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP) and levels of copper (Cu) and ferritin were increased significantly in plasma of alcohol, thermally oxidised PUFA (DeltaPUFA) and alcohol + DeltaPUFA groups, which were decreased significantly on treatment with both the doses of ferulic acid. The activities of enzymic antioxidants viz. superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and non enzymic antioxidants like vitamin C, vitamin E, and reduced glutathione (GSH) and the levels of zinc (Zn) were significantly decreased in alcohol, DeltaPUFA and alcohol + DeltaPUFA groups which were improved significantly on treatment with both the doses of FA. The reduction in oxidative stress was more significant in 20 mg/kg body weight treatment groups compared to 40 mg/kg body weight. Thus from the results obtained, we conclude that FA effectively protects the system against alcohol and PUFA induced oxidative stress.
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PMID:Influence of ferulic acid on circulatory prooxidant-antioxidant status during alcohol and PUFA induced toxicity. 1538 26

The present study was undertaken to evaluate the effects of curcumin and curcumin analog on blood oxidant-antioxidant status during nicotine-induced toxicity in male Wistar rats. Lung toxicity was induced by subcutaneous injection of nicotine at a dose of 2.5 mg/kg of body weight (5 days a week, for 22 weeks). The enhanced circulatory lipid peroxides in nicotine-treated rats was accompanied by a significant decrease in the levels of ascorbic acid, vitamin E, reduced glutathione, glutathione peroxidase, superoxide dismutase, and catalase. There was a reduction in the levels of zinc with an elevation of copper and ferritin in nicotine-treated rats. Administration of curcumin and curcumin analog significantly lowered the lipid peroxidation and enhanced the antioxidant status with modulation in the levels of zinc, copper, and ferritin. However, the effect was more significant in curcumin analog-treated rats than in curcumin-treated rats. The results of the present study suggest that curcumin and curcumin analog exert their protective effects by modulating the extent of lipid peroxidation and enhancing the antioxidant status.
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PMID:Inhibition of nicotine-induced toxicity by curcumin and curcumin analog: a comparative study. 1567 91

The analysis of vitamin and iron indexes of 95 children sufficiently supplied with vitamin C and vitamin B2 and carotenoids deficiency has been carried out. Vitamin E deficit takes place among anemic children (with decreased hemoglobin blood level) 2 fold more often than among healthy children. From another side, decreased hemoglobin blood level, erythrocyte quantity and erythrocyte indexes have been determined 1.7-2.4 fold more often in insufficiently supplied with vitamin E children. Tocopherols serum level had tendency to the decrease and vitamin E deficit took place 2 fold more frequently in children suffering from iron deficiency anemia that is with decreased hemoglobin and serum ferritin concentrations. Marked positive linear correlation between these iron indexes and vitamin E serum level has been revealed. These results give evidence concerning significant role of this vitamin in the body iron supplying. The results obtained give evidence for multi-deficient anemia presence among children, which are not always caused by iron deficit. High frequency of vitamin E and B group vitamins deficiency proves expediency of these vitamins inclusion in complex therapy of iron deficiency.
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PMID:[The connection between vitamin and iron status indexes of school-age children]. 1568 56

The hypothesis according to which iron overload could be harmful has been extensively and controversially discussed in the literature. One underlying pathological mechanism may be elevated oxidative stress. Thus, we studied the correlation between hemochromatosis and an established marker of oxidative stress, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha, iPF2alpha-III, 15-F2t-IsoP). We enrolled 21 patients with hemochromatosis, positive for the homozygous C282Y mutation in the HFE gene, and 21 healthy controls frequency-matched by age and gender in a case-control study design. The objective was to show that iron overload in HFE-related hemochromatosis is associated with increased oxidative stress assessed through 8-iso-PGF(2alpha) urinary excretion, and that oxidative stress is impacted by iron-removal treatment (phlebotomy). Study parameters were transferrin saturation, 8-iso-PGF(2alpha) urine excretion, transferrin, ferritin, serum iron, and vitamins A and E for all participants. Iron concentration in the liver and non-transferrin-bound iron were measured in patients only. We found a significant difference in 8-iso-PGF2alpha in patients (245 [interquartile range 157-348] pg/mg creatinine) compared with controls (128 [106-191] pg/mg creatinine, P = 0.002). Vitamin A was significantly reduced in cases (0.34 [0.25-1.83] microg/ml compared to 3.00 [2.11-3.39] microg/ml, P < 0.001), while vitamin E did not show a significant difference in cases (14.7 [11.5-18.1] microg/ml) compared with controls (14.9 [13.1-19.2] microg/ml, P = 0.52). After phlebotomy treatment and normalization of the iron parameters in the hemochromatosis group, serum vitamin A levels were significantly increased (1.36 [1.08-1.97] microg/ml, P = 0.035 vs. baseline, P < 0.001 vs. controls) and 8-iso-PGF2alpha urinary excretion was lowered to control levels (146 [117-198] pg/mg creatinine, P = 0.38 vs. controls). In our study, HFE-related hemochromatosis was associated with increased oxidative stress and hypovitaminemia A in C282Y homozygotes. The increased oxidative stress was reversible by normalization of the iron load by phlebotomy. Thus, phlebotomy is an effective and adequate means for reducing oxidative stress in these patients.
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PMID:Increased urinary excretion of 8-iso-prostaglandin F2alpha in patients with HFE-related hemochromatosis: a case-control study. 1654 87

Patients with alcoholic liver disease frequently exhibit iron overload in association with increased hepatic fibrosis. Even moderate alcohol consumption elevates body iron stores; however, the underlying molecular mechanisms are unknown. Hepcidin, a circulatory peptide synthesized in the liver, is a key mediator of iron metabolism. Ethanol metabolism significantly down-regulated both in vitro and in vivo hepcidin mRNA and protein expression. 4-Methylpyrazole, a specific inhibitor of the alcohol-metabolizing enzymes, abolished the effects of ethanol on hepcidin. However, ethanol did not alter the expression of transferrin receptor1 and ferritin or the activation of iron regulatory RNA-binding proteins, IRP1 and IRP2. Mice maintained on 10-20% ethanol for 7 days displayed down-regulation of liver hepcidin expression without changes in liver triglycerides or histology. This was accompanied by elevated duodenal divalent metal transporter1 and ferroportin protein expression. Injection of hepcidin peptide negated the effect of ethanol on duodenal iron transporters. Ethanol down-regulated hepcidin promoter activity and the DNA binding activity of CCAAT/enhancer-binding protein alpha (C/EBPalpha) but not beta. Interestingly, the antioxidants vitamin E and N-acetylcysteine abolished both the alcohol-mediated down-regulation of C/EBPalpha binding activity and hepcidin expression in the liver and the up-regulation of duodenal divalent metal transporter 1. Collectively, these findings indicate that alcohol metabolism-mediated oxidative stress regulates hepcidin transcription via C/EBPalpha, which in turn leads to increased duodenal iron transport.
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PMID:Alcohol metabolism-mediated oxidative stress down-regulates hepcidin transcription and leads to increased duodenal iron transporter expression. 1725 19

beta-thalassemia is the most common monogenic hereditary blood disease in children. It is also considered to be the regional pathology for Georgia. The influence of iron metabolism disorder on metabolic processes taking place in erythrocyte membrane and their role in pathogenesis of beta-thalassemia, is very important until now. The aim of our research was to study the condition of oxidoreduction processes in RBC membranes on the background of iron metabolism disorder in children with beta-thalassemia. We observed 44 patients with beta-thalassemia aged 0.4-14 years. Iron, ferritin, malon-dialdehyde and catalase were evaluated. The carried out investigation revealed, that oxidoreduction processes in patients with beta-thalassemia, together with iron overload, is one of the factors in promoting further disorder of proliferation and differentiation processes in erythrone system and also in formation of ineffective erythropoiesis. The revealed changes in data of iron metabolism. malon-dialdehyde and catalase showed us the need for correction of this disorder. Pathogenetically there are good reasons to include in the combined treatment beta-thalassemia the membrano-protective preparations (vitamin E, acetylcysteine) together with the hemotransfusion and chelator therapy.
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PMID:[Damage of iron metabolism and oxidoreduction process in children with beta-thalassemia]. 1690 50

The accumulation of oxidatively damaged proteins is a well-known hallmark of aging and several neurodegenerative diseases including Alzheimer's, Parkinson's and Huntigton's diseases. These highly oxidized protein aggregates are in general not degradable by the main intracellular proteolytic machinery, the proteasomal system. One possible strategy to reduce the accumulation of such oxidized protein aggregates is the prevention of the formation of oxidized protein derivatives or to reduce the protein oxidation to a degree that can be handled by the proteasome. To do so an antioxidative strategy might be successful. Therefore, we undertook the present study to test whether antioxidants are able to prevent the protein oxidation and to influence the proteasomal degradation of moderate oxidized proteins. As a model protein we choose ferritin. H2O2 induced a concentration dependent increase of protein oxidation accompanied by an increased proteolytic susceptibility. This increase of proteolytic susceptibility is limited to moderate hydrogen peroxide concentrations, whereas higher concentrations are accompanied by protein aggregate formation. Protective effects of the vitamin E derivative Trolox, the pyridoindole derivative Stobadine and of the standardized extracts of flavonoids from bark of Pinus Pinaster Pycnogenol and from leaves of Ginkgo biloba (EGb 761) were studied on moderate damaged ferritin.
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PMID:Ferritin oxidation and proteasomal degradation: protection by antioxidants. 1698 94


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