• Proceedings of the Korean Radioactive Waste Society Conference
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• 2005.06a
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• pp.513-517
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• 2005

This study examined the possibility of using striped field mice as a biological dosimeter or indicator for the environmental radio-surveillance. For this study, the external morphological characteristics and isoenzymic types of dark-striped field mice were studied after they were captured. Among the morphological external characteristics, the dark-brown coat, dark back stripe, head-to-tail length, tail length, and ear length matched the taxonomical characteristics of dark-striped field mice. The analyses on L-lactate dehydrogenase, aspartate aminotransferase, and malate dehydrogenese revealed that one species of dark-striped field mice, called Apodemus agrarius, was inhabitated throughout a wide range of Korea. On the other hand, A. agrarius and ICR mice to analyze their survival rate and frequency of micronuclei in peripheral polychromatic erythrocytes after irradiation (0, 0.5, 1, 3, 5, 7, 9 Gy). The $LD_{50/30}$ of A. agrarius and ICR mice were approximately 5 Gy and 7Gy, respectively. The results of the study reveal that wild A. agrarius have a high potential as a biological monitoring system to determine the impact of radiation effect in areas such as those within the vicinity of nuclear power plants.

• Archives of Pharmacal Research
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• v.22 no.5
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• pp.479-484
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• 1999

In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on isolated heart perfusion model. Hearts were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, $37^{\circ}C$) on a Langendroff apparatus. After equilibration, isolated hearts were treated with UDCA 20 to 160 $\mu$M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. After global ischemia (30 min), ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular developed pressure, coronary flow, double product and time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 21.4 min during ischemia, LVDP was 18.5 mmHg at the endpoint or reperfusion and LDH activity in total reperfusion effluent was 54.0 U/L. Cardioprotective effects of UDCA against ischemia/reperfusion consisted of a reduced TTC $(EC_{25}=97.3{\mu}M)$, reduced LDH release and enhanced recovery of cardiac contractile function during reperfusion. Especially, the treatments of UDCA 80 and $160 {\mu}M $ significantly increased LVDP and reduced LDH release. Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage.

• Journal of Environmental Science International
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• v.28 no.2
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• pp.249-257
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• 2019

Ulmus davidiana Nakai (UDN) has been traditionally used as a herbal medicine to treat inflammatory diseases in Korea. In the present study, we investigated the anti-ecotoxic potential of a 116 kDa glycoprotein isolated from UDN (UDN glycoprotein) in human intestinal epithelial INT-407 cells. We demonstrated that UDN glycoprotein ($20{\mu}g/mL$) could inhibit the production of lactate dehydrogenase (LDH) induced by toluene, an ecotoxic substance. Additionally, we found that the toluene-induced intestinal cytotoxicity was mediated by the phosphorylation of p38 Mitogen-Activated Protein Kinase (MAPK) via the production of intracellular Reactive Oxygen Species (ROS). The UDN glycoprotein significantly decreased the levels of ROS production and p38 MAPK activation in toluene-stimulated INT-407 cells. Moreover, the UDN glycoprotein inhibits the phosphorylation of nuclear factor-kappa B ($NF-{\kappa}B$), which is responsible for the production of LDH, in toluene-stimulated INT-407 cells. Collectively, our data indicate that UDN glycoprotein is a natural antioxidant and a modulator of ecotoxicity signaling pathways in human intestinal epithelial cells.

• Toxicological Research
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• v.35 no.3
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• pp.233-239
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• 2019

Nerium oleander (N. oleander) is a well-known poisonous shrub that is frequently grown in gardens and public areas and contains numerous toxic compounds. The major toxic components are the cardiac glycosides oleandrin and neriin. The aim of our study was to evaluate the toxic effects of an ethanolic N. oleander leaf extract on haematological, cardiac, inflammatory, and serum biochemical parameters, as well as histopathological changes in the heart. N. oleander extract was orally administered for 14 and 30 consecutive days at doses of 100 and 200 mg of dried extract/kg of body weight in 0.5 mL of saline. The results showed significant increases in mean corpuscular volume, white blood cell counts, platelet counts, interleukins (IL-1 and IL-6), tumour necrosis factor alpha, C reactive protein, alanine aminotransferase, lactate dehydrogenase, creatine kinase and creatine kinase MB, especially at high doses. Marked pathological changes were perceived in the heart tissue. Thus, it can be concluded that exposure to N. oleander leaf extract adversely affects the heart and liver.

• Clinical and Experimental Pediatrics
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• v.59 no.7
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• pp.308-311
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• 2016

We report a human parechovirus-3 (HPeV-3) infection in 2 neonates who had prolonged fever (>5 days) with palmar-plantar erythema. This distinctive rash was observed 4-5 days after fever onset, just before defervescence. Elevated aspartate aminotransferase, lactate dehydrogenase, and ferritin levels were characteristic laboratory findings in the 2 cases, suggesting tissue damage caused by hypercytokinemia. Case 1 was treated with intravenous immunoglobulin, considering the possibility of severe systemic inflammatory responses. The initial ferritin level was 385 ng/mL (range, 0-400 ng/mL); however, the level increased to 2,581 ng/dL on day 5 after fever onset. Case 2 presented with milder clinical symptoms, and the patient recovered spontaneously. HPeV-3 was detected in cerebrospinal fluid and/or blood samples, but no other causative agents were detected. The findings from our cases, in accordance with recent studies, suggest that clinical features such as palmar-plantar erythema and/or hyperferritinemia might be indicators of HPeV-3 infection in neonates with sepsis-like illness. In clinical practice, where virology testing is not easily accessible, clinical features such as palmar-plantar erythema and/or hyperferritinemia might be helpful to diagnose HPeV-3 infection.

• Korean Journal of Agricultural Science
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• v.44 no.4
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• pp.586-594
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• 2017

Mitochondrial activity affects skeletal muscle energy metabolism and phenotype. To address whether mitochondrial activity can modulate muscle phenotype in vitro, protein expression of myosin heavy chain (MyHC) in C2C12 muscle cell lines was investigated after treated with antimycin A, an inhibitor of oxidative phosphorylation in mitochondria. Fully differentiated C2C12 myotubes were administrated with different concentration of antimycin A including 0, 100, 200, 500, 700, and 1000 ng/mL. After 72 h treatment, myosin heavy chain isoform expression and related enzyme activity (lactate dehydrogenase; LDH and creatine kinase) were analyzed. Administration of antimycin A changed expression of MyHC in C2C12 myotubes showing a shift from slow to fast twitching muscle type. Protein expression of MyHC type 2b (fast twitching muscle type) was decreased (P < 0.05) by antimycin A treatment (500, 700, and 1000 ng/mL) when compared with control group. Administration of antimycin A (1000 ng/mL), however, decreased (P < 0.05) MyHC type I (slow twitching muscle type). Interestingly, LDH activity was increased (P < 0.05) by antimycin A treatment. Results from our current study proposed a possibility that skeletal muscle phenotype, including MyHC and LDH activity, can be shifted from slow to fast twitching type by inhibiting the mitochondrial activity in C2C12 myotubes.

• Journal of Applied Biological Chemistry
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• v.59 no.3
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• pp.173-178
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• 2016

Phenyllactic acid (PLA), which is a known antimicrobial compound, can be synthesized through the reduction of phenylpyruvic acid (PPA) by lactate dehydrogenase of lactic acid bacteria (LAB). PLA-producing LAB was isolated from coffee beans, and the isolated LAB was identified as Lactobacillus zeae Y44 by 16S rRNA gene sequence analysis. Cell-free supernatant (CFS) from L. zeae Y44 was assessed for both its capability to produce the antimicrobial compound PLA and its antifungal activity against three fungal pathogens (Rhizoctonia solani, Botrytis cinerea, and Colletotrichum aculatum). PLA concentration was found to be 4.21 mM in CFS when L. zeae Y44 was grown in MRS broth containing 5 mM PPA for 12 h. PLA production could be promoted by the supplementation with PPA and phenylalanine (Phe) in the MRS broth, but not affected by 4-hydroxy-phenylpyruvic acid, and inhibited by tyrosine as precursors. Antifungal activity assessment demonstrated that all fungal pathogens were sensitive to 5 % CFS (v/v) of L. zeae Y44 with average growth inhibitions ranging from 27.8 to 50.0 % (p<0.005), in which R. solani was the most sensitive with an inhibition of 50.0 %, followed by B. cinerea and C. aculatum. However, pH modification of CFS to pH 6.5 caused an extreme reduction in their antifungal activity. These results may indicate that the antifungal activity of CFS was caused by acidic compounds like PLA or organic acids rather than proteins or peptides molecules.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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• pp.233-239
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• 1998

Stimulated alveolar macrophages and neutrophils produce nitric oxide, a free radical by an inducible nitric oxide synthase(iNOS), which reacts with superoxide anion to form peroxynitrite, a more highly reactive toxic species. The objectives of the present study were to evaluate acute inflammatory lung injury and to determine iNOS mRNA induction and nitric oxide production by rat broncho-alveolar lavage cells following intratracheal treatment of silica. After 4 h exposure to silica, differential counts of broncho-alveolar lavage cells and lactate dehydrogenase(LDH) activity as well as total protein in the broncho-alveolar lavage fluid were determined. Broncho-alveolar lavage cells were also assayed for iNOS mRNA and the productions of nitrite and nitrate measured in the cells cultured. Differential analysis of broncho-alveolar lavage cells showed that the number of alveolar macrophages slightly decreased following silica treatment; however, red blood cells, lymphocytes, and neutrophils significantly were increased by 9-, 14-, and 119-fold following silica treatment, respectively, compared with the saline control. It was also found significant increases in the LDH activity and total protein in the lavage fluid obtained from silica-treated rats, indicating silica-induced acute lung injury. Northern blot analysis demonstrated that the steady state levels of iNOS mRNA in broncho-alveolar lavage cells were increased following silica treatment. The productions of nitrite and nitrate in the cultured cells were significantly increased by 2-fold following silica treatment, respectively, which were attenuated by the NOS inhibitor $N{\omega}-nitro-L-arginine-methyl$ ester(L-NAME) and partially reversed by L-arginine. These findings suggest that nitric oxide production in alveolar macrophages and recruited neutrophils is increased in response to silica. Nitric oxide may contribute in part to acute inflammatory lung injury.

• International Journal of Oral Biology
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• v.34 no.2
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• pp.97-103
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• 2009

L-trans-pyrrolidine-2,4-dicarboxylate (PDC) is a potent inhibitor of glutamate transporters. In our current study, we investigated whether the neuronal death induced by PDC involves mechanisms other than excitotoxicity in mixed mouse cortical cultures. Cortical cultures at 13-14 days in vitro were used and cell death was assessed by measuring the lactate dehydrogenase efflux into bathing media. Glutamate and PDC both induced neuronal death in a concentration-dependent manner but the neurotoxic effects of glutamate were found to be more potent than those of PDC. Treatment with 10, 100 and 200 ${\mu}$M PDC equally potentiated 50 ${\mu}$M glutamate-induced neuronal death. The neuronal death induced by 75 ${\mu}$M glutamate was almost abolished by treatment with the NMDA antagonists, MK-801 and AP-5, but was unaffected by NBQX (an AMPA antagonist), trolox (antioxidant), BDNF or ZVAD-FMK (a pan-caspase inhibitor). However, the neuronal death induced by 200 ${\mu}$M PDC was partially but significantly attenuated by single treatments with MK-801, AP-5, trolox, BDNF or ZVAD-FMK but not NBQX. Combined treatments with MK-801 plus trolox, MK-801 plus ZVAD-FMK or MK-801 plus BDNF almost abolished neuronal death, whereas combined treatments with trolox plus ZVADFMK, trolox plus BDNF or ZVAD-FMK plus BDNF did not enhance the inhibitory action of any single treatment with these drugs. These results demonstrate that the neuronal death induced by PDC involves not only in the excitotoxicity induced by the accumulation of glutamate but also the oxidative stress induced by free radical generation. This suggests that apoptotic neuronal death plays a role in PDCinduced oxidative neuronal injury.

• Food Science and Biotechnology
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• v.16 no.2
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• pp.260-264
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• 2007

Gleditsiae Semen (GS) has been used in both Korea and China as herbal medicine for the treatment of cephalalgia, catharsis, and other diseases. However, the apoptosis of GS against human cancer cells has not previously been investigated. The primary objective of this study was to determine the mechanisms inherent in GS-induced cytotoxicity and apoptosis, using methanolic extract of GS (GSE) in HT-29 human colon carcinoma cells. We found that GSE induced cytotoxicity in HT-29 cells in a dose-dependent manner, and this effect was verified via a lactate dehydrogenase release assay and a colony formation assay. In particular, HT-29 cells showed extensive cell death when treated with $50\;{\mu}g/mL$ of GSE; the calculated $IC_{50}$ value was $20\;{\mu}g/mL$. It induced characteristic apoptotic signs in HT-29 cells, including chromatin condensation and DNA fragmentation, occurring within 6-24 hr when the cells were treated at a concentration of $50\;{\mu}g/mL$. Interestingly, we detected the activation of caspase-3 and -9, but not caspase-8, and apoptotic bodies in GSE-treated HT-29 cells. Collectively, our results indicate that GSE induces apoptosis via a mitochondria-mediated apoptotic pathway, and these findings may be significant with regard to the development of a new drug for the treatment of human colon carcinoma cells.