• Journal of Nutrition and Health
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• v.35 no.2
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• pp.223-228
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• 2002

The purpose of this study was to investigate the relationship between iron deficiency without anemia and physical performance in healthy women aged 20-21 yrs. Ten subjects with normal iron stores (serum ferritin $\geq$ 12$\mu\textrm{g}$/L: iron-sufficient group) and 11 subjects with iron depletion without anemia (serum ferritin < 12 $\mu\textrm{g}$/L and serum hemoglobin > 120 g/L: iron-depleted group) were chosen from a group of 50 women and were given physical-performance tests, including determinations of maximum oxygen consumption (VO$_2$ max) and ventilatory threshold. Iron status assessment included determination of hemoglobin, hematocrit, seam ferritin, total iron-binding rapacity, serum iron and transferrin saturation values. Dietary iron intake was assessed based on seven-day food intake records written by the subjects. Physical activity level was estimated by frequency questionnaires and two-week physical activity records were compiled daily by the subjects. Blood ferritin concentration was significantly lower in the iron-depleted group than in the iron-sufficient group (p < 0.05). However, other variables showing iron status was not different between the groups. There were no significant differences in body size, body composition and physical activity levels between the groups. Daily dietary iron, total protein and animal protein intakes of the iron-sufficient group were significantly higher than those of the iron depleted group. However, no differences were found in the amount of dietary vitamin C and fiber between the groups. The values for VO$_2$max and VO$_2$max corrected with weight or fat-free mass were not different between the groups. However, the ventilatory threshold was significantly higher in the iron sufficient group than in the iron-depleted group. The lower ventilatory threshold in the iron-depleted group suggests that iron depletion without anemia could diminish aerobic physical performance in young women. In addition, a significant correlation of physical performance to serum fferritin level was shown only in the iron depleted group.

• Journal of Nutrition and Health
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• v.40 no.4
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• pp.362-370
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• 2007

The study was designed to assess the effect of iron and cereal supplementation on children's iron nutritional status in social welfare institutions. Dietary survey was carried out methods of food weighing and record by interview (n=74). A nutritional intervention study was carried out through supplementing iron supplements and cereal for 4 weeks in 4-12 years old children. Children received daily 40 mg elemental Fe as iron protein succinylate (n=23) and 3.6 mg elemental Fe as 100 g cereal (n=24), respectively. Blood samples were drawn before and after supplementation. Nutrients which children's intake was less than two-thirds of the RDA were vitamin A, vitamin B-1, vitamin B-2, calcium and iron. The mean daily intake of iron was 5.1 mg for male and 4.9 mg for female, and 52.3% for male and 45.4% for female of Korean RDA. The proportion of children with iron depletion assessed by TIBC (> 360 ${\mu}g$/dl) and serum ferritin (< 20 ng/ml) were 56.6% and 58.7%, respectively. The proportion of children with the iron deficient erythropoiesis assessed by serum iron (< 70 ${\mu}g$/dl), Hb (< 12 g/dl), Hct (< 36%) were 76.0%, 58.7%, 64.0%, respectively. After iron supplements treatment, Hb (p<0.001), Hct(p<0.001), serum iron (p<0.001), transferrin saturation (p<0.001) and serum ferritin (p<0.Ol) increase significantly and only TIBC decreased slightly. After cereal supplementation, in anemic children, Hct (p<0.001), serum iron (p<0.001) and transferrin saturation (p<0.001) were significantly increased. The effect of iron supplements and cereal supplementation in children with iron deficient erythropoiesis were more effective to improve the iron nutritional status than children with iron depletion. It was concluded that cereal supplementation program in anemic children was also effective to improve iron nutritional status.

• Environmental Analysis Health and Toxicology
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• v.19 no.4
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• pp.359-366
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• 2004

Iron (Fe) is an essential metal in biological processes, which maintains a homeostasis in the human body. Divalent metal transporter 1 (DMT1) has been known as an iron transporting membrane protein, which is involved in the uptake Fe at the apical portion of intestinal epithelium, and may transport Fe across the membrane of acidified endosome in peripheral tissues. In this study, we studied the tissue distribution of DMT1 in the Fe supplemented (FeS) diet fed rats, and the regulation of DMT1 expression by depleting body Fe. Sprague-Dawley rats were divided into two groups, and fed FeS (120 mg Fe/kg) diet or Fe deficient (FeD, 2∼6 mg Fe/kg) diet for 4 weeks. The evaluation of body Fe status was monitored by measuring sFe, UIBC and tissue Fe concentration. Additionally, DMT1 mRNA levels were analyzed in the peripheral tissues by using the quantitative real time RT-PCR method. In the FeS diet fed rats, the tissue Fe was maintained at a relatively high level, and DMT1 was eventually expressed in all tissues studied. DMT1 was highly expressed in the testis, kidney and spleen, while a moderate levels of DMT1 expression was detected in the brain, liver and heart. In the digestive system, the highest level of DMT1 was found in the duodenum. Feeding the FeD diet caused a reduced body weight gain and depletion of body Fe with finding of decreased sFe, increased UIBC and decreased tissue Fe concentration. The depletion of body Fe upregulated DMT1 expression in the peripheral tissue. The expression of DMT1 was very sensitive to the body Fe depletion in the small intestine, especially in the duodenum, showing dramatically higher levels in the FeD rats than those of the FeS group. In the FeD diet fed animals, the expression of DMT1 was low significantly in other tissues compared with the duodenum. The expression of DMT1, however, was 60∼120% higher in the testis, kidney and spleen, and 30∼50% higher in the lung, liver and heart, compared to the FeS diet fed rats. In summary, DMT1 expression was ubiquitous in mammalian tissue, and the level of expression was the organ-dependent. The expression of DMT1 in peripheral tissues was upregulated by depletion of body Fe. Duodenum was the most sensitive tissue among organs studied during Fe depletion, and expressed the greatest level of DMT1, while other tissues were less higher than in duodenum. This study supports that DMT1 plays a role in maintaining the body Fe level through intestinal uptake as well as homeostasis of Fe in the peripheral tissue.

• Journal of the Korean Society of Food Culture
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• v.18 no.6
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• pp.575-583
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• 2003

To evaluate the effect of cereal supplementation on children's iron nutritional status of Korean institutionalized was designed. Dietary survey was carried out methods of food weighting in the breakfast or/and dinner, and record interview in lunch (n=74). A nutritional intervention study was carried out through supplementing cereal for 4 weeks in 24 children of 1 institution from 4 to 12 years. The children received 3.6mg elemental Fe(as 100g cereal) per day. Blood samples were drawn before and after supplementation. Nutrients which children's intake was less than two-thirds of Korean RDA were Vit A, Vit B1, Vit B2, Ca and Fe. The mean daily intakes of iron were 5.1mg for male and 4.9mg for female and 52.3% for male and 45.4% for female of Korean RDA. The proportions of children with iron depletion assessed by TIBC(>360mg/dl) and serum ferritin(<20ng/ml) were 56.6% and 58.7%, respectively. The proportions of children with the iron deficient erythropoiesis assessed by serum iron(<70ml/dl), Hb(<12g/dl), and Hct(<36%) were 76.0%, 58.7%, and 64.0%, respectively. After cereal supplementation, in anemic children, levels of Hct(p<0.001), serum iron(p<0.001) and transferrin saturation(p<0.001) were significantly increased. The effect of cereal supplementation in children with iron deficient erythropoeisis was more effective to improve the iron nutritional status than children with iron depletion. It was concluded that cereal supplementation program in anemic children was also effective to improve iron nutritional status.

• 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.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.9 no.2
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• pp.129-138
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• 2006

Lots of cases relating Helicobacter pylori infection to iron-deficiency anemia have been described in the literature and H. pylori infection has emerged as a cause of refractory iron-deficiency anemia which is unresponsive to oral iron therapy. H. pylori-associated iron-deficiency anemia can be treated by H. pylori eradication. It is not thought to be attributable to gastrointestinal blood loss, such as duodenal ulcer. The mechanism by which H. pylori infection contributes to iron-deficiency anemia remains unclear. However, four possible explanations can be posited for this relationship; occult blood loss secondary to chronic gastritis, reduced iron absorption due to hypo- or achlorhydria, increased iron consumption by H. pylori, and iron sequestration in gastric mucosa. H. pylori-associated iron-deficiency anemia seems to develop in populations at increased risk for iron depletion. When pubescent girls, including athletes, are found to have iron-deficiency anemia refractory to iron administration, they should be evaluated for H. pylori infection.

• Proceedings of the Korean Society of Toxicology Conference
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• 2005.05a
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• pp.145-145
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• 2005

• Corrosion Science and Technology
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• v.3 no.6
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• pp.227-232
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• 2004

The carboxylates as a corrosion inhibitor has been studied by many researchers because of its environmental safety and low depletion rate. However, conventional test methods of inhibitor such as weight loss measurements, linear polarization resistance and corrosion potential monitoring etc., evaluate uniform corrosion of metals. These methods are unable to evaluate crevice-related corrosions, which are encountered in most of heat exchanging facilities. In order to choose the optimum corrosion inhibitor, the appropriate test methods are required to evaluate their performances in service environment. From this point of view, polarization technique was used to evaluate the characteristics of sodium heptanoate on corrosion behavior for carbon steel. Especially a thin film crevice sensor technique were applied to simulate the crevice corrosion in this study. From these experiments, we found that oxygen as an oxidizing agent was required to obtain stable passive film on the metal. Presence of oxygen, however, accelerated crevice corrosion. Potential shift by oxygen depletion and weakened inhibitive film inside the crevice were responsible for such accelerated feature. It is shown that film for corrosion inhibition is a mixture of sodium heptanoate and iron (II) heptanoate as reaction product of iron surface and sodium heptanoate. The iron (II) heptanoate which has been synthesized by reaction of heptanoic acid and ferrous chloride in methanol solution forms bidentate complex.

• BMB Reports
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• v.40 no.1
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• pp.82-87
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• 2007

Our heterologous expression system of the human ferritin H-chain gene (hfH) allowed us to characterize the cellular effects of ferritin in yeasts. The recombinant Saccharomyces cerevisiae (YGH2) evidenced impaired growth as compared to the control, which was correlated with ferritin expression and with the formation of core minerals. Growth was recovered via the administration of iron supplements. The modification of cellular iron metabolism, which involved the increased expression of high-affinity iron transport genes (FET3 and FTR1), was detected via Northern blot analysis. The findings may provide some evidence of cytosolic iron deficiency, as the genes were expressed transcriptionally under iron-deficient conditions. According to our results examining reactive oxygen species (ROS) generation via the fluorescence method, the ROS levels in YGH2 were decreased compared to the control. It suggests that the expression of active H-ferritins reduced the content of free iron in yeast. Therefore, present results may provide new insights into the regulatory network and pathways inherent to iron depletion conditions.

• Animal cells and systems
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• v.6 no.2
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• pp.171-180
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• 2002

Nitric oxide has high affinity for iron, and thus it can cause intracellular iron loss. We tested the idea that intracellular iron can be the primary target of NO toxicity by comparing the signaling mechanisms involved in cell death caused by iron depletion and that caused by NO. Treatment of HL-60 cells with a NO donor, S-nitroso-N-acetyl-DL-penicillamine (SNAP), decreased the intracellular iron level rapidly as that observed with the iron chelator deferoxamine (DFO). Iron chelators such as DFO and mimosine could induce death of human leukemic HL-60 cells by a mechanism requiring activation of p38 kinase, c-Jun N-terminal kinase, caspase-3 and caspase-8. DFO and SNAP also caused release of cytochrome c from mitochondria. Inhibition of p38 kinase by a selective inhibitor, SB203580, abolished the NO and DFO-induced cell death, release of cytochrome c, and activation of caspase-3 and caspase-8, thus indicating that p38 kinase lies upstream in the cell death processes. In a parallel situation, the cells that are sensitive to NO showed similar sensitivity to DFO. Moreover, simultaneous addition of ferric citrate, an iron-containing compound, inhibited the SNAP and DFO-induced activation of caspases and also blocked the NO-mediated cell cycle arrest at $G_1$ phase. Collectively, our data implicate that the NO-induced cell death of tumor cells including HL-60 cells is mediated by depletion of iron and further suggest that activation of p38 kinase lies upstream of cytochrome c release and caspase activation involved in this apoptotic process.