• Korean Journal of Community Nutrition
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• v.2 no.3
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• pp.267-274
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• 1997

The purpose of this study was to determine the proportion of 5th grade school children with iron depletion or iron depleted anemia with simultaneously assessing their general nutritional status. The anthropometric measurements, nutrient intake, and biochemical status of iron were measured for 261 school children from 5th grade residing in low income area of Pucheon. The mean height and weight of male were 138.7cm and 33.6kg respectively and were significantly lower than those of female. Mean fat percent, triceps skinfolds thickness and arm circumference were 21.4$\%$, 13.7mm and 22.2cm for female and were significantly higher than 19.1$\%$, 11.4mm, 21.4cm of male respectively. The intake on vitamin A and calcium were 46.4$\%$ and 47.7$\%$ of RDA for male and 36.6$\%$ and 44.9$\%$ for male respectively. The energy intake, carbohydrate, thiamin, niacin, ascorbic acid of male were significantly higher than those of female respectively. The mean daily intake of iron were 7.5mg for male and 7.3mg for female and were not significantly different. The mean biochemical indices of iron nutritional status were not significantly different between male and female expect free erythrocyte protoporphyrin(FEP) and FEP : hemoglobin ratio. The proportion of male assessed by serum iron(<70$\mu\textrm{g}$/㎗), Hb($\%$), FEP(<70$\mu\textrm{g}$/㎗RBC) were 25.4$\%$, 8.4$\%$. 0.8$\%$, 1.8$\%$ respectively and 23.2$\%$, 8.4$\%$, 3.4$\%$, 1.0$\%$ for female respectively.

• Analytical Science and Technology
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• v.14 no.1
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• pp.72-79
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• 2001

Oxidative decomposition of 2, 4, 6-trichlorophenol(TCP) was studied in aqueous solution. Iron and manganese protoporphyrin [or tetrakis(p-carboxyphenylporphyrin)] and their polymer supported derivatives were used as catalysts, and $KHSO_5$ and tert-butyldroperoxide(TBHP) as oxidants. Metalloporphyrin itself shows very poor catalytic activity in oxidative decomposition of TCP with oxidant. However, very high catalytic activity was observed when metalloporphyrin was chemically bound to newly synthesized polymers or XAD2 resin. Additionally, it revealed much higher catalytic activity in the presence of water-soluble polymers having a electron-donating axial ligand such as pyridine and immidazole. Maleic acid and chloromaleic acid were found in the resulting solution by ESI-MS. Especially, XAD2-supported metalloporphyrins can be reused as catalysts due to insolubility to solvent, and stability against oxidant.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.10 no.2
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• pp.165-172
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• 2000

This study was carried out to investigate relationship between plasma $\delta$ - aminolevulinic acid (ALAP) and lead exposure indices in exposure to lead. The subjects were 218 male workers in 2 storage battery companies and 2 secondary smelting companies. Blood lead(PbB), blood zinc-protoporphyrin( ZPP), urinary $\delta$ - aminolevulinic acid (ALAU), hemoglobin(Hb), and hematocrit(Hct) were measured as lead exposure indices. The results were as follows, 1. The means of blood lead and blood ZPP concentration of subjects were $27.2{\pm}14.0{\mu}g/d{\ell}$ and $55.1{\pm}47.6{\mu}g/d{\ell}$, respectively. The means of plasma $\delta$ - ALA and urinary $\delta$ - ALA concentration were $18.9{\pm}25.1{\mu}g/d{\ell}$ and $2.1{\pm}4.6mg/{\ell}$, respectively. 2. The concentration of ALAP was $11.2{\mu}g/{\ell}$ for below $20{\mu}g/d{\ell}$ PbB, $12.8{\mu}g/{\ell}$ for from $21-40{\mu}g/d{\ell}$ PbB, and $51.2{\mu}g/{\ell}$ for over $40{\mu}g/d{\ell}$ PbB, respectively. 3. ALAP was significantly correlated with ALAU(r=0.829, p<0.01), ZPP(r=0.724, p<0.01) and PbB(r=0.552, p<0.01).

• Asian-Australasian Journal of Animal Sciences
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• v.29 no.11
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• pp.1664-1674
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• 2016

This research analyzed the effect of ${\beta}$-glucan that is expected to alleviate the production of the inflammatory mediator in macrophagocytes, which are processed by the lipopolysaccharide (LPS) of Escherichia. The incubated layer was used for a nitric oxide (NO) analysis. The DNA-binding activation of the small unit of nuclear factor-${\kappa}B$ was measured using the enzyme-linked immunosorbent assay-based kit. In the RAW264.7 cells that were vitalized by Escherichia coli (E. coli) LPS, the ${\beta}$-glucan inhibited both the combatant and rendering phases of the inducible NO synthase (iNOS)-derived NO. ${\beta}$-Glucan increased the expression of the heme oxygenase-1 (HO-1) in the cells that were stimulated by E. coli LPS, and the HO-1 activation was inhibited by the tin protoporphyrin IX (SnPP). This shows that the NO production induced by LPS is related to the inhibition effect of ${\beta}$-glucan. The phosphorylation of c-Jun N-terminal kinases (JNK) and the p38 induced by the LPS were not influenced by the ${\beta}$-glucan, and the inhibitory ${\kappa}B-{\alpha}$ ($I{\kappa}B-{\alpha}$) decomposition was not influenced either. Instead, ${\beta}$-glucan remarkably inhibited the phosphorylation of the signal transducer and activator of transcription-1 (STAT1) that was induced by the E. coli LPS. Overall, the ${\beta}$-glucan inhibited the production of NO in macrophagocytes that was vitalized by the E. coli LPS through the HO-1 induction and the STAT1 pathways inhibition in this research. As the host immune response control by ${\beta}$-glucan weakens the progress of the inflammatory disease, ${\beta}$-glucan can be used as an effective immunomodulator.

• BMB Reports
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• v.41 no.2
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• pp.164-169
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• 2008

The tumor suppressor gene p53 regulates apoptotic cell death and the cell cycle. In this study, we investigated the role of p53 in nitric oxide (NO)-induced apoptosis in vascular smooth muscle cells (VSMCs). We found that the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) increased apoptotic cell death in p53-deficient VSMCs compared with wild-type cells. The heme oxygen-ase (HO) inhibitor tin protoporphyrin IX reduced the resistance of wild-type VSMCs to SNAP-induced cell death. SNAP promoted HO-1 expression in both cell types. HO-2 protein was increased only in wild-type VSMCs following SNAP treatment; however, similar levels of HO-2 mRNA were detected in both cell types. SNAP significantly increased the levels of non-heme-iron and dinitrosyl iron-sulfur clusters in wild-type VSMCs compared with p53-deficient VSMCs. Moreover, pretreatment with FeSO4 and the carbon monoxide donor CORM-2, but not biliverdin, significantly protected p53-deficient cells from SNAP-induced cell death compared with normal cells. These results suggest that wild-type VSMCs are more resistant to NO-mediated apoptosis than p53-deficient VSMCs through p53-dependent up-regulation of HO-2.

• Nutrition Research and Practice
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• v.8 no.4
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• pp.352-359
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• 2014

BACKGROUND/OBJECTIVES: In this study, we determined the anti-inflammatory activities and the underlying molecular mechanisms of the methanol extract from Erigeron Canadensis L. (ECM) in LPS-stimulated RAW264.7 macrophage cells. MATERIALS/METHODS: The potential anti-inflammatory properties of ECM were investigated by using RAW264.7 macrophages. We used western blot assays and real time quantitative polymerase chain reaction to detect protein and mRNA expression, respectively. Luciferase assays were performed to determine the transactivity of transcription factors. RESULTS: ECM significantly inhibited inducible nitric oxide synthase (iNOS)-derived NO and cyclooxygenase-2 (COX-2) derived PGE2 production in LPS-stimulated RAW264.7 macrophages. These inhibitory effects of ECM were accompanied by decreases in LPS-induced nuclear translocations and transactivities of $NF{\kappa}B$. Moreover, phosphorylation of mitogen-activated protein kinase (MAPKs) including extracellular signal-related kinase (ERK1/2), p38, and c-jun N-terminal kinase (JNK) was significantly suppressed by ECM in LPS-stimulated RAW264.7 macrophages. Further studies demonstrated that ECM by itself induced heme oxygenase-1 (HO-1) protein expression at the protein levels in dose-dependent manner. However, zinc protoporphyrin (ZnPP), a selective HO-1 inhibitor, abolished the ECM-induced suppression of NO production. CONCLUSIONS: These results suggested that ECM-induced HO-1 expression was partly responsible for the resulting anti-inflammatory effects. These findings suggest that ECM exerts anti-inflammatory actions and help to elucidate the mechanisms underlying the potential therapeutic values of Erigeron Canadensis L.

• BMB Reports
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• v.46 no.8
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• pp.410-415
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• 2013

Adhesion molecules such as ICAM-1 are important in the infiltration of leukocytes into the site of inflammation. In this study, we investigated the inhibitory effects of curcumin on ICAM-1 expression and monocyte adhesiveness as well as its underlying action mechanism in the TNF-${\alpha}$-stimulated keratinocytes. Curcumin induced expression of heme oxygenase-1 (HO-1) in the human keratinocyte cell line HaCaT. In addition, curcumin induced Nrf2 activation in dose- and time-dependent manners in the HaCaT cells. Curcumin suppressed TNF-${\alpha}$-induced ICAM-1 expression and subsequent monocyte adhesion, which were reversed by the addition of tin protoporphyrin IX (SnPP), a specific inhibitor of HO-1, or HO-1 knockdown using siRNA. Furthermore, Nrf2 knockdown using siRNA reversed the inhibitory effect of curcumin on the TNF-${\alpha}$-induced ICAM-1 expression and adhesion of monocytes to keratinocytes. These results suggest that curcumin may exert its anti-inflammatory activity by suppressing the TNF-${\alpha}$-induced ICAM-1 expression and subsequent monocyte adhesion via expression of HO-1 in the keratinocytes.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.2
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• pp.83-88
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• 2011

A large body of evidence has indicated that induction of endogenous antioxidative proteins seems to be a reasonable strategy for delaying the progression of cell injury. In our previous study, cilostazol was found to increase the expression of the antioxidant enzyme heme oxygenase-1 (HO-1) in synovial cells. Thus, the present study was undertaken to examine whether cilostazol is able to counteract tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-induced cell death in endothelial cells via the induction of HO-1 expression. We exposed human umbilical vein endothelial cells (HUVECs) to TNF-${\alpha}$ (50 ng/ml), with or without cilostazol ($10{\mu}M$). Pretreatment with cilostazol markedly reduced TNF-${\alpha}$-induced viability loss in the HUVECs, which was reversed by zinc protoporphyrine IX (ZnPP), an inhibitor of HO-1. Moreover, cilostazol increased HO-1 protein and mRNA expression. Cilostazol-induced HO-1 induction was markedly attenuated not only by ZnPP but also by copper-protoporphyrin IX (CuPP). In an assay measuring peroxisome proliferator-activated receptor-${\gamma}$ (PPAR-${\gamma}$) transcription activity, cilostazol directly increased PPAR-${\gamma}$ transcriptional activity which was completely abolished by HO-1 inhibitor. Furthermore, increased PPAR-${\gamma}$ activity by cilostazol and rosiglitazone was completely abolished in cells transfected with HO-1 siRNA. Taken together, these results indicate that cilostazol up-regulates HO-1 and protects cells against TNF-${\alpha}$-induced endothelial cytotoxicity via a PPAR-${\gamma}$-dependent pathway.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2015.10a
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• pp.958-960
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• 2015

Sickle cells possess a unique combination of traits that may enable their use as models for novel synthetic tumor targeting controlled release drug carriers with the ability to treat disseminated tumors in advanced metastatic disease. In this study, we assess the ability of light-activated release sickle cells to enhance tumor delivery of the fluorescent dye calcein by delayed photolysis controlled release compared to free systemic administration of calcein. Sickle cells from mouse models of the disease were shown to preferentially accumulate in tumors compared to adjacent tissue, in 4T1 tumors in mice on a time scale about 12 hours. Sickle cells photosensitized with protoporphyrin IX achieved delayed release of 50% of contents 8-16 hours after photoactivation, which was deemed useful for in vivo delivery of cargo to tumors given the tumor accumulation time of the sickle cells. Sickle cells may be useful as a model for new synthetic drug carrier particles with delayed photolysis controlled release properties.

• Korean Journal of Weed Science
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• v.14 no.3
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• pp.176-183
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• 1994

This study was conducted to investigate how KC6361, a new type diphenylether compound inducing bleaching, increase the greening of cucumber cotyledon in darkness. Protoporphyrin IX formation, reaccumulation rate of protochlorophyllide(Pchlide) in darkness after phototransformation and Shibata shift were not affected. Whereas, aminolevulinic acid(ALA), protochlorophyll and chlorophyll were increased, and especially protochlorophyll was significantly accumulated. When KC6361 and phytol were applied alone or in combination with ALA, the transformation from Pchlide into protochlorophyll was accelerated in darkness. These results suggest that the greening of the etiolated cucumber cotyledon treated with KC6361 seems to be caused by the accumulation of phytol or/and Geranylgeranylpyrophosphate and their increased esterification with Pchlide in darkness.