• Journal of Crop Science and Biotechnology
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• v.10 no.2
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• pp.64-72
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• 2007

Iron is an important micronutrient for plants. Iron metabolism is a complex mechanism under a delicate balance. Iron metabolism represents two major problems for plants: deficiency as a consequence of solubility problems and toxicity due to excess solubility in anaerobic conditions. In the last few years, new genes have been discovered that influence iron uptake, transport and storage. Irrigated rice is exposed to high levels of $Fe^{II}$, normally rare in aerobic soil conditions. The implications of altering iron uptake rates and the effects of newly discovered genes are discussed.

• Journal of Microbiology and Biotechnology
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• v.30 no.8
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• pp.1142-1148
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• 2020

Mitochondria play a vital role in iron uptake and metabolism in pathogenic fungi, and also influence virulence and drug tolerance. However, the regulation of iron transport within the mitochondria of Cryptococcus neoformans, a causative agent of fungal meningoencephalitis in immunocompromised individuals, remains largely uncharacterized. In this study, we identified and functionally characterized Mrs3/4, a homolog of the Saccharomyces cerevisiae mitochondrial iron transporter, in C. neoformans var. grubii. A strain expressing an Mrs3/4-GFP fusion protein was generated, and the mitochondrial localization of the fusion protein was confirmed. Moreover, a mutant lacking the MRS3/4 gene was constructed; this mutant displayed significantly reduced mitochondrial iron and cellular heme accumulation. In addition, impaired mitochondrial iron-sulfur cluster metabolism and altered expression of genes required for iron uptake at the plasma membrane were observed in the mrs3/4 mutant, suggesting that Mrs3/4 is involved in iron import and metabolism in the mitochondria of C. neoformans. Using a murine model of cryptococcosis, we demonstrated that an mrs3/4 mutant is defective in survival and virulence. Taken together, our study suggests that Mrs3/4 is responsible for iron import in mitochondria and reveals a link between mitochondrial iron metabolism and the virulence of C. neoformans.

• Journal of Nutrition and Health
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• v.37 no.4
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• pp.273-280
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• 2004

This study was conducted to examine the effect of dietary iron levels on lipid metabolism, antioxidative and antithrombogenic capacities in 16-month-old rats. Thirty-two Sprague-Dawley male 16-month-old rats weighing 618 $\pm$ 6 g were raised for 10 days with medium-iron diet (35 ppm in diet) and blocked into 4 groups according to their body weights. One of groups was sacrificed to obtain initial data and the rest 3 groups were raised for 3 months with experimental diets containing different levels of iron (5 ppm, 35 ppm, and 350 ppm). Total lipid, triglyceride and total chole-sterol concentrations in plasma and liver, HDL-cholesterol concentration in plasma, fecal total lipid triglyceride and total cholesterol excretions, thiobarbituric acid reactive substances (TBARS) level in plasma LDL + VLDL (low density lipoprotein + very low density lipoprotein) fractions, blood-clotting time and eicosanoids levels in plasma were measured. The results are as follows: Plasma total lipid, triglyceride and total cholesterol concentrations, TBARS level in plasma LDL + VLDL fractions were increased and blood-clotting time tended to be shortened during 3 months of experimental period. Low (5 ppm) iron diet improved lipid metabolism via increasing HDL-cholesterol and fecal choles-terol excretion. High (350 ppm) iron diet decreased plasma total lipid, triglyceride and total cholesterol concentrations as compared to medium (35 ppm) iron diet and lowered body weight and epididymal fat pad weight. On the other hand, TBARS level in plasma LDL + VLDL fractions and blood-clotting time were increased with high iron diet. It is plausible that low iron diet improves lipid metabolism, antioxidative and antithrombogenic capacities in 16-month-old rats.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.3
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• pp.638-641
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• 2006

Iron is the required microelement supporting life and is the main component of hemoglobin. Thus iron has affinity with exercise capacity. Iron metabolism turbulence induced by exercise is one of causes of hematopoietic hypofunction. Results of the experiment showed that long-term treadmill exercise of progressive loading significantly decreased levels of erythrocyte indexes, serum iron, serum ferritin and significantly increased serum transferrin level. Nutrition supplement could significantly retard the variations, and Exercise +Nutrition group have higher levels of erythrocyte indexes, serum iron, serum ferritin and lower level of serum transferrin than Exercise group. The results indicated that nutrition supplement have function of prevent and cure on iron metabolism turbulence induced by exercise, furthermore significantly enhance hemoglobin level in rats.

• Journal of Applied Biological Chemistry
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• v.42 no.2
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• pp.62-65
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• 1999

Iron regulatory proteins (IRPs) 1 and 2 bind with equally high affinity to specific RNA stem-loop sequences known as iron-responsive elements (IRE) which mediate the post-transcriptional regulation of many genes of iron metabolism. To study putative IRE-like sequences in RNA transcripts using the IRP-IRE interaction, Eight known genes from database were selected and the RNA binding activity of IRE-like sequences were compared to IRP-2. Among them, the IRE-like sequence in 3'-untranslational region (UTR) of divalent ration transporter-1 (DCT-1) shows a significant RNA binding affinity. This finding predicts that IRE consensus sequence present within 3'-UTR of DCT-1 might confer the regulation by IRP-2.

• Journal of Nutrition and Health
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• v.29 no.7
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• pp.713-720
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• 1996

To study the effect of caffeine intake levels on iron metabolism, the iron utilization, iron contents of serum, liver, spleen, kidney, hemoglobin and hematocrit were compared in rats of different sex fed various levels of caffeine (3.5 and 7.0mg/100g body weight) for three weeks. There were no significant caffeine induced differences in feed intake, body weight gain but feed intake of male rats were significantly lower than that of female rats. Hemoglobin, hematocrit and iron contents of the serum were not significantly different between caffeine free and caffeine groups or male and female rats. Iron contents of kidney were decreased by elevation of injected caffeine levels rather than those of liver and spleen. caffeine male groups showed more increased uine volume, urinary and fecal excretions of iron than caffeine free or caffeine female groups. Apparent digestibility and retention of iron were significantly decreased by increment of injected caffeine levels. Male rate rats were more susceptible to injected caffeine on iron excretion than female rats. Current findings suggest that excessive caffeine consumption can affect iron excretion via urine and feces thereby decrease the utilization of iron, and have more significant effect on male than female rats.

• Journal of Microbiology and Biotechnology
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• v.18 no.8
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• pp.1368-1376
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• 2008

In our previous study, the expression of active H-ferritins in Saccharomyces cerevisiae was found to reduce cell growth and reactive oxygen species (ROS) generation upon exposure to oxidative stress; such expression enhanced that of high-affinity iron transport genes (FET3 and FTR1). The results suggested that the recombinant cells expressing H-ferritins induced cytosolic iron depletion. The present study analyzes metabolic changes under these circumstances via proteomic methods. The YGH2 yeast strain expressing A-ferritin, the YGH2-KG (E62K and H65G) mutant strain, and the YGT control strain were used. Comparative proteomic analysis showed that the synthesis of 34 proteins was at least stimulated in YGH2, whereas the other 37 proteins were repressed. Among these, the 31 major protein spots were analyzed via nano-LC/MS/MS. The increased proteins included major heat-shock proteins and proteins related to endoplasmic reticulum-associated degradation (ERAD). On the other hand, the proteins involved with folate metabolism, purine and methionine biosynthesis, and translation were reduced. In addition, we analyzed the insoluble protein fractions and identified the fragments of Idh1p and Pgk1p, as well as several ribosomal assembly-related proteins. This suggests that intracellular iron depletion induces imperfect translation of proteins. Although the proteins identified above result from changes in iron metabolism (i.e., iron deficiency), definitive evidence for iron-related proteins remains insufficient. Nevertheless, this study is the first to present a molecular model for iron deficiency, and the results may provide valuable information on the regulatory network of iron metabolism.

• Nutrition Research and Practice
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• v.2 no.4
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• pp.317-321
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• 2008

Macrophages play a key role in iron metabolism by recycling iron through erythrophagocytosis. Ferroportin-l (FPN1) is a transporter protein that is known to mediate iron export from macrophages. Since divalent metals often interact with iron metabolism, we examined if divalent metals could regulate the expression of FPN1 in macrophages. J774 macrophage cells were treated with copper, manganese, zinc, or cobalt at 10, 50, or $100\;{\mu}M$ for 16 to 24 h. Then, FPN1 mRNA and protein levels were determined by quantitative real-time PCR and Western blot analyses, respectively. In addition, effects of divalent metals on FPN1 promoter activity were examined by luciferase reporter assays. Results showed that copper significantly increased FPN1 mRNA levels in a dose-dependent manner. The copper-induced expression of FPN1 mRNA was associated with a corresponding increase in FPN1 protein levels. Also, copper directly stimulated the activity of FPN1 promoter-driven reporter construct. In contrast, manganese and zinc had no effect on the FPN1 gene expression in J774 cells. Interestingly, cobalt treatment in J774 cells decreased FPN1 protein levels without affecting FPN1 mRNA levels. In conclusion, our study results demonstrate that divalent metals differentially regulate FPN1 expression in macrophages and indicate a potential interaction of divalent metals with the FPN1-mediated iron export in macrophages.

• Journal of Sport and Applied Science
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• v.6 no.4
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• pp.11-23
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• 2022

New insights into the aetiology of anaemia in athletes have been discovered in recent years. From hemodilution and redistribution, which are thought to commit to so-called "sports anaemia," to iron deficiency triggered by higher requirements, dietary requirements, decreased uptake, enhanced losses, hemolysis, and sequester, to genetic factors of different types of anaemia (some related to sport), anaemia in athletes necessitates a careful and multisystem methodology. Dietary factors that hinder iron absorption and enhance iron bioavailability (e.g., phytate, polyphenols) should be considered. Celiac disease, which is more common in female athletes, may be the consequence of an iron deficiency anaemia that is unidentified. Sweating, hematuria, gastrointestinal bleeding, inflammation, and intravascular and extravascular hemolysis are all ways iron is lost during strength training. In training, evaluating the iron status, particularly in athletes at risk of iron deficiency, may work on improving iron balance and possibly effectiveness. Iron status is influenced by a healthy gut microbiome. To eliminate hemolysis, athletes at risk of iron deficiency should engage in non-weight-bearing, low-intensity sporting activities.

• Journal of Applied Biological Chemistry
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• v.66
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• pp.159-164
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• 2023

Ferroptosis is a type of regulated cell death recently discovered, characterized by the accumulation of iron-dependent lipid peroxides in the cell membrane, and it involves a complex network of signaling pathways, including iron metabolism, lipid peroxidation, and redox regulation. The dysregulation of these pathways can lead to the induction of ferroptosis and the development of liver diseases, such as alcoholic liver disease, non-alcoholic fatty liver disease, viral hepatitis, and liver cancer. Studies have demonstrated that targeting key molecules involved in iron metabolism, lipid peroxidation, and redox regulation can reduce liver injury and improve liver function in different liver diseases by inhibiting ferroptosis. Thus, modulation of ferroptosis presents a promising therapeutic target for treating liver diseases. However, further research is required to gain a more comprehensive understanding of the mechanisms underlying the role of ferroptosis in liver diseases and to develop more effective and targeted treatments.