Ferritin and the response to oxidative stress

Orino, Koichi; Lehman, L; Tsuji, Yoshiaki; Ayaki, Hitoshi; Torti, Suzy V.; Torti, Frank M.

doi:10.1042/0264-6021:3570241

Cited by 279 publications

(165 citation statements)

References 42 publications

(57 reference statements)

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“…The system is sensitive not only to iron availability but also to the oxidative status of the cell. In fact, ferritin can be viewed both as part of a group of iron regulatory proteins that include transferrin and the transferrin receptor (TfR) and as a member of the protein family that orchestrates the cellular defense against stress and inflammation, as outlined in several reviews [26,27,28,29]. These reviews focus on the molecular mechanisms and biological implications of ferritin regulation by cytokines, oxidants, oncogenes, growth factors, and other stimuli, as well as their relevance to the complex.…”

Section: Regulation Of Ferritinmentioning

confidence: 99%

Importance of Ferritin for Optimizing Anemia Therapy in Chronic Kidney Disease

et al. 2010

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The clinical significance of serum ferritin in monitoring the iron status of patients on maintenance hemodialysis (MHD) has become suspected. In this review, we reassess the interpretation of high serum ferritin values in such patients, with the goal of treating their anemia in a safe way. From the observations that (1) H-ferritin gene transcription is predominantly active in inflammatory conditions, whereas L-ferritin is induced only after exposure to very high iron concentrations and is preferentially secreted to plasma from hepatocytes; (2) the expression of both types of ferritin proteins are exclusively dependent on intracellular free iron, which is often sequestered by LPS or cytokines in several cell types, and (3) splenic iron is depleted and serum ferritin does not increase in the combined conditions of both inflammation and iron deficiency, it is deduced that elevated serum ferritin levels are caused by the accumulation of intracellular iron, especially reticuloendothelial cells or macrophages, hepatocytes, and other cells, while cytokines or inflammation might modulate the relative ratio of ferritin to body iron storage. Therefore, high levels of serum ferritin in patients on MHD can be used to indicate iron deposition in most cells, including vascular and immunocompetent cells, and is still a reliable indicator of the need to withhold iron administration.

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Section: Regulation Of Ferritinmentioning

confidence: 99%

Importance of Ferritin for Optimizing Anemia Therapy in Chronic Kidney Disease

et al. 2010

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“…The expression of iron storage protein, ferritin, is induced by oxidative stress as an antioxidant, indicating that ferritin has a dual function to store iron in a bioavailable and nontoxic form, as iron (Fe 2+ ) produces the most toxic hydroxyl radical through the Fenton reaction [17,20]. On the other hand, cytoprotection of ferritin against oxidative stress is controversial due to the release of Fe 2+ by superoxide anion and/ or radical products [7,22], suggesting that intracellular ferritin protein and iron levels may affect the detoxification capacity of ROS.…”

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confidence: 99%

Effects of Oxidative Stress Caused by <i>tert</i>-Butylhydroquinone on Cytotoxicity in MDCK Cells

Shibuya

Kobayashi

Yoshikawa

et al. 2012

The Journal of Veterinary Medical Science

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ABSTRACT. Antioxidant and oxidative stress effects of prooxidants are generally dose-dependent, and these effects depend on the prooxidant species and cell type. However, the cellular response to oxidant challenge is a complicated interplay of events involving cellular expression of phase II detoxification enzymes and cellular metal metabolism. This study demonstrates the effect of tertbutylhydroquinone (t-BHQ)-induced oxidative stress on MDCK cells. Cell toxicity tests were carried out using the crystal violet (CV) assay with the following prooxidants: t-BHQ, diethyl maleate (DEM), hydrogen peroxide (H 2 O 2 ), diquat (DQ) and β-naphthoflavone (β-NF). Except for β-NF, these prooxidants showed dose-dependent cytotoxicity besides the most potent t-BHQ cytotoxicity. Only t-BHQ and DEM caused significant time-dependent expression of ferritin protein as an antioxidant, which segregates Fe 2+ , causing the Fenton reaction. t-BHQ and DEM increased formation of lipid peroxidation, but DQ showed a tendency to decrease lipid peroxidation levels. In XTT assay, even when substantial cell death was observed in the CV assay, t-BHQ appeared to increase cell viability by enhancing XTT reduction, likely through the production of NADPH. Although curcumin, which induces cytoprotective phase II enzymes and chelates metal irons, decreased cell viability, it inhibited t-BHQ cytotoxicity. These results indicate that t-BHQ exhibits strong cytotoxicity against MDCK cells, an effect mitigated by curcumin, and that t-BHQ-induced oxidative stress activates the pentose phosphate pathway.

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“…While some studies have shown negative effects of iron on oxidative stress biomarkers, the incidence of some kinds of cancers and the risk of acute myocardial infarction [28,29,30], other studies have shown a positive role of iron and its related factors, such as ferritin, in the human body [31,32,33,34]. For that reason, we measured several parameters of oxidative stress in our study sample.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Consequences of Iron-Fortified Flour Consumption in Nonanemic Men

Pouraram¹,

Elmadfa²,

Dorosty³

et al. 2012

Ann Nutr Metab

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Background/Aims: Despite the advantages of fortifying flour with iron, there are still special concerns regarding the possible adverse effects of the extra iron consumed by nonanemic individuals. This study aimed to investigate the oxidative stress and iron status following 8 and 16 months of consumption of iron-fortified flour in nonanemic men. Methods: In a before-and-after intervention study, 78 nonanemic apparently healthy 40- to 65-year-old men were randomly selected from Semnan, in the northeast of Iran. Data were collected at three time points. Evaluation of oxidative stress biomarkers as well as the assessment of iron status was performed in all three stages. After baseline data collection, the flour fortification program was started with 30 mg/kg iron as ferrous sulfate. Results: After 16 months, serum iron levels had significantly increased from 102.9 ± 31.5 µg/dl (baseline) to 117.2 ± 29.8 µg/dl (p < 0.001). The mean total antioxidant capacity (1.71 ± 0.10 µM) was significantly lower than that at baseline (1.83 ± 0.17 µM; p < 0.01). Among other oxidative stress biomarkers, only superoxide dismutase and glutathione peroxidase activity increased significantly compared to the beginning of the study (p < 0.001 and p < 0.001, respectively). The results of this study did not show any symptoms of iron overload after 8 and 16 months. Conclusions: Our data did not support the safety of flour fortification with 30 mg/kg iron as ferrous sulfate as a community-based approach to control iron deficiency in nonanemic healthy men.

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Ferritin and the response to oxidative stress

Cited by 279 publications

References 42 publications

Importance of Ferritin for Optimizing Anemia Therapy in Chronic Kidney Disease

Importance of Ferritin for Optimizing Anemia Therapy in Chronic Kidney Disease

Effects of Oxidative Stress Caused by <i>tert</i>-Butylhydroquinone on Cytotoxicity in MDCK Cells

Long-Term Consequences of Iron-Fortified Flour Consumption in Nonanemic Men

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