• 한국식품위생안전성학회지
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• 제14권2호
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• pp.160-166
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• 1999

Microbial populations of total aerobic bacteria and coliforming bacteria, TBA, Hunter's color value, heme pigments, muscle protein solubility, cooking loss and shear force were investigated fro evaluating the shelf life of chicken legs gamma-irradiated at doses of 1, 3, 5 and 10 kGy with air-contained and vacuum-packaged methods. The initial microbial populations decreased with gamma irradiation depending upon the dose, and microorganisms in the vacuum-packaged samples were inhibited more than those in the air-contained samples. Hunter's L and a values of the surface and inside of the legs increased by gamma irradiation, showing a bright red color and the red color was maintained during the storage of both samples. The concentrations of oxymyoglobin among the heme pigments increased by gamma irradiation. Muscle protein solubility slightly increased by increasing the applied dose. There were no significant differences in the cooking loss and shear force values. In conclusion, the combination of gamma irradiation and vacuum-packaging could extend the shelf life of chilled chicken without deterioration of the quality.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2001년도 추계학술대회 및 정기총회
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• pp.94-94
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• 2001

Prostaglandin endoperoxide H synthase (PGHS) catalyzes the committed step in prostaglandins and thromboxane A$_2$-- oxygenation of arachidonic acid to the hydroperoxy endoperoxide PGG$_2$, followed by reduction PGG$_2$to the alcohol PGH$_2$. The two reactions by PGHS -- cyclooxygenase and peroxidase -- occur at distinct but structurally and functionally interconnected sites. The peroxidase reaction occurs at a heme-containing active site located near the protein surface. The cyclooxygenase reaction occurs in a hydrophobic channel in the core of the enzyme. Initially a peroxide reacts with the heme group, yielding Compound I and an alcohol derived from the oxidizing peroxide. Compound I next undergoes an intramolecular reduction by a single electron traveling from Tyr385 along the peptide chain to the proximal heme ligand, His388, and finally to the heme group. Following the binding of arachidonic acid, Tyr385 tyrosyl radical initiates the cyclooxygenase reaction by abstracting the 13-pro(5) hydrogen atom to give an arachidonyl radical, which sequentially reacts with two molecules of oxygen to yield PGG$_2$. In order to characterize PGHS peroxidase active site, we examined various lipid peroxides with purified recombinant ovine PGHS proteins and determined the rate constants. The results have shown that twenty-carbon unsaturated fatty acid hydroperoxides have similar efficiency in peroxidation by PGHS, irrespective of either the location of hydroperoxy group or the number of double bonds. It was also confirmed by the subsequent study with PGHS peroxidase active site mutants.

• BMB Reports
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• 제41권2호
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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.

• Journal of Nutrition and Health
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• 제33권2호
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• pp.167-178
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• 2000

The effect of oral vitamin e (800IU/day) and C (500mg/day) supplementation for 10 days and/or smoking cessation for 5 days on oxidative damage to the red blood cells (RBC) of male smokers (22.2$\pm$0.2 years old) was studied. RBC were tested for their ability to protect against smoking-induced oxidative damage by measuring heme proteins (carboxyhemoglobin, hemoglobin, methemoglobin, oxyhemoglobin), hemolysis and thiobarbiturinc acid reactive substances (TBARS). Plasma levels of vitamin c, A, E, $\beta$-catotene, total cholesterol, glutamic pyruvic transaminase(GPT) and glutamic oxaloacetic transaminase(GOT) were also analyzed. In experiment one, a comparison was made of heme proteins and lipid damage to RBC, plasma antioxidant status (indexed by plasma levels of vitamin C, E, A and $\beta$-carotene) between smokers(n=56) and non-smokers (n=16). No differences were found in plasma antioxidant status, heme protein damage and TBARS concentration of RBC. In experiment two, 46 fasting male smokers from experiment one were divided into 4 groups. The groups were smoking with placebo group(SP, n=14), smoking cessation with vitamins supplementatin group (SV, n=13), smoking cessation with placebo group (NSP, n=9) and smoking cessation with vitamins supplementation group (NSV, n=10). After supplementing antioxidant vitamins, significant increases were seen in plasma vitamins supplementation group (NSV, n=10). After supplementing antioxidant vitamins, significant increases were seen plasma vitamin C (p<0.05) and vitamin E levels (p<0.05). The plasma vitamin E level was highest in the NSV group. Vitmain E and C supplementation provided some protection against heme proteins and lipid damage by lowering methemoglobin, hemolysis and TBARS concentration of RBC. Smoking cessation significantly decreased TBARS of RBC and plasma total cholesterol concentration. Supplementing vitamin E and C with smoking cessation considerably lowered plasma total cholesterol. These results point to a special association among smoking, oxidative damage and plasma antioxidant vitamin status. They indicate that increases in plasma antioxidant status can be detected after the supplementation of vitamin C and E and that smoking cessation had an additional effect on plasma vitamin E level. The present data suggest that improved antioxidant status induced by antioxidant supplementation or smoking cessation may help prevent oxidative damage in smokers.

• BMB Reports
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• 제53권4호
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• pp.212-217
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• 2020

Activation of peroxisome proliferator-activated receptor γ (PPARγ) serves as a key factor in the proliferation and invasion of breast cancer cells and is a potential therapeutic target for breast cancer. However, the mechanisms underlying this effect remain largely unknown. Heme oxygenase-1 (HO-1) is induced and over-expressed in various cancers and is associated with features of tumor aggressiveness. Recent studies have shown that HO-1 is a major downstream target of PPARγ. In this study, we investigated the effects of induction of HO-1 by PPARγ on TPA-induced MMP-9 expression and cell invasion using MCF-7 breast cancer cells. TPA treatment increased NF-κB /AP-1 DNA binding as well as MMP-9 expression. These effects were significantly blocked by 15d-PGJ₂, a natural PPARγ ligand. 15d-PGJ₂ induced HO-1 expression in a dose-dependent manner. Interestingly, HO-1 siRNA significantly attenuated the inhibition of TPA-induced MMP-9 protein expression and cell invasion by 15d-PGJ₂. These results suggest that 15d-PGJ₂ inhibits TPA-induced MMP-9 expression and invasion of MCF-7 cells by means of a heme oxygenase-1-dependent mechanism. Therefore, PPARγ/HO-1 signaling-pathway inhibition may be beneficial for prevention and treatment of breast cancer.

• Bulletin of the Korean Chemical Society
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• 제23권8호
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• pp.1073-1077
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• 2002

Binding of dodecyl trimethylammonium bromide (DTAB) to human and bovine hemoglobin and globin samples has been investigated in 50 mM glycine buffer pH = 10, I = 0.0318 and 300 K by equilibrium dialysis and temperature scanning spectrophotometry techniques and method for calculation of average hydrophobicity. The binding data has been analyzed, in terms of binding capacity concept $({\theta})$, Hill coefficient (nH) and intrinsic Gibbs free energy of binding $({\Delta}Gbv).$ The results of binding data, melting point (Tm) and average hydrophobicity show that human hemoglobin has more structural stability than bovine hemoglobin sample. Moreover the results of binding data analysis represent the systems with two and one sets of binding sites for hemoglobin and globin, respectively. It seems that the destabilization of hemoglobin structure due to removal of heme group, is responsible of such behavior. The results indicating the removal of heme group from hemoglobin caused the depletion of first binding set as an electrostatic site upon interaction with DTAB and exposing the hydrophobic patches for protein.

• 동의생리병리학회지
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• 제25권5호
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• pp.843-848
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• 2011

In Korea, China, and Japan, Paeonia lactiflora Pall (PL) has been used in the treatment of rheumatoid arthritis, hepatitis, and fever for more than 1200 years. It has been reported that PL has protective effects against $H_2O_2$-induced oxidative stress and LPS-induced liver inflammation. However cellular and molecular mechanism of PL protection against oxidative stress has not fully been elucidated. Here, we describe that the water-soluble extract of PL decreased $H_2O_2$-induced hepatotoxicity. This hepatoprotective effect of PL is reason to decrease the level of intracellular reactive oxygen species (ROS) and increase expression of heme oxygenase 1 (HO-1) and heat shock protein 72 (HSP72) which proteins are involved in protecting the cells from stress like as oxidative stress. We also elucidated that hepatoprotective effect of PL was abolished by knock down of HO-1 and HSP72 by siRNA. These results suggest that the increasing of HO-1 and HSP72 protein by PL treatment might be participated in hepatoprotective effect against oxidative stress such as $H_2O_2$.

• Asian-Australasian Journal of Animal Sciences
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• 제20권7호
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• pp.1120-1126
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• 2007

An iron-fortified whey protein concentrate (Fe-WPC) was prepared by addition of ferric chloride to concentrated whey. A large part of the iron in the Fe-WPC existed as complexes with proteins such as ${\beta}$-lactoglobulin. The bioavailability of iron from Fe-WPC was evaluated using iron-deficient rats, in comparison with heme iron. Rats were separated into a control group and an iron-deficiency group. Rats in the control group were given the standard diet containing ferrous sulfate as the source of iron throughout the experimental feeding period. Rats in the iron-deficiency group were made anemic by feeding on an Fe-deficient diet without any added iron for 3 wk. After the iron-deficiency period, the iron-deficiency group was separated into an Fe-WPC group and a heme iron group fed Fe-WPC and hemin as the sole source of iron, respectively. The hemoglobin content, iron content in liver, hemoglobin regeneration efficiency (HRE) and apparent iron absorption rate were examined when iron-deficient rats were fed either Fe-WPC or hemin as the sole source of iron for 20 d. Hemoglobin content was significantly higher in the rats fed the Fe-WPC diet than in rats fed the hemin diet. HRE in rats fed the Fe-WPC diet was significantly higher than in rats fed the hemin diet. The apparent iron absorption rate in rats fed the Fe-WPC diet tended to be higher than in rats fed the hemin diet (p = 0.054). The solubility of iron in the small intestine of rats at 2.5 h after ingestion of the Fe-WPC diet was approximately twice that of rats fed the hemin diet. These results indicated that the iron bioavailability of Fe-WPC was higher than that of hemin, which seemed due, in part, to the different iron solubility in the intestine.

• 한국미생물·생명공학회지
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• 제41권2호
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• pp.253-262
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• 2013

In this study, we analyzed the anti-oxidative and anti-inflammatory activities of seven medicinal herbs. All extracts of the tested herbs, Euryale ferox Salisbury, Echinops setifer Iljin, Amomum cardamomum Linne, Tetrapanax papyriferus, Illicium verum Hook. f., Typha orientalis Presl, and Piper longum Linne, exhibited potent anti-oxidative activity as confirmed by DPPH radical scavenging capacity. Lipopolysaccharide (LPS) induced nitric oxide (NO) production, in the RAW 264.7 cell line, was also ameliorated by all extracts' treatments in a dose dependent manner. NO suppressive activity originated from the inhibition of inducible nitric oxide synthase (iNOS) protein expression by the extracts. Three extracts, E. ferox S., I. verum Hook. f., and P. longum L., possessed suppressive activity against, not only iNOS, but also cycloxygenase 2 (COX-2) protein expression. These three extracts may then serve as potential candidates for non steroidal analgesic inflammation drugs (NSAIDs). Furthermore, all extracts induced anti-oxidative enzyme, heme oxygenase 1, protein expression. Taken together, these results provide an important new insight into the fact that various medicinal herbs possess potent anti-oxidative and anti-inflammatory activities and might be utilized as promising agents in the field of health products. Further studies for the identification of the active compounds from medicinal herbs are clearly needed.

• The Korean Journal of Physiology and Pharmacology
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• 제15권4호
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• pp.203-210
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• 2011

Cilostazol is a selective inhibitor of phosphodiesterase 3 that increases intracellular cAMP levels and activates protein kinase A, thereby inhibiting vascular smooth muscle cell (VSMC) proliferation. We investigated whether AMP-activated protein kinase (AMPK) activation induced by heme oxygenase-1 (HO-1) is a mediator of the beneficial effects of cilostazol and whether cilostazol may prevent cell proliferation and reactive oxygen species (ROS) production by activating AMPK in VSMC. In the present study, we investigated VSMC with various concentrations of cilostazol. Treatment with cilostazol increased HO-1 expression and phosphorylation of AMPK in a dose- and time-dependent manner. Cilostazol also significantly decreased platelet-derived growth factor (PDGF)-induced VSMC proliferation and ROS production by activating AMPK induced by HO-1. Pharmacological and genetic inhibition of HO-1 and AMPK blocked the cilostazol-induced inhibition of cell proliferation and ROS production.These data suggest that cilostazol-induced HO-1 expression and AMPK activation might attenuate PDGF-induced VSMC proliferation and ROS production.