• Journal of Sasang Constitutional Medicine
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• v.11 no.2
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• pp.283-299
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• 1999

1. Purpose : Systemic injection of kainic acid in experimental animals induces the limbic seizure and structural damages in hippocampus and amygdala which resembles the changes in human temporal lobe epilepsy. The author performed this study to investigate the neuroprotective effects of Yuldahansotang, on the neurotoxicity induced by kainic acid in the hippocampus in rats. 2. Method : Kainic acid was administered intraperitoneally. And feeding with Yuldahansotang for 3 weeks after kainic acid administration. Seizure were induced in male mice (kainate 10-40 mg/kg i.p) and animals were sacrified at various time-points after injection. The experimental animals were sacrificed at 1, 2, 3day and 1, 3weeks while Yuldahansotang administrations. Seizure were graded using a behavioral scale developed in our laboratory. c-fos belong to immediate early genes(IEGs) known to have rapid and brief responses. And neuronal injury was assayed by examining DNA fragmentation using in situ nick translation histochemistry. 3. Results & Conclusion : Seizure severity paralled kainate dosage. At higher doses DNA fragmentation is seen mainly in hippocampus in area CA3, and variable in CA1, thalamus, amygdala within 24 h, is maximal within 72 h, and is large gene by 7 days after administration of kainate. And we can't see the expression of DNA fragmentation and c-fos in the mice what feeded by Yuldahansotang after 7 days from kainic acid administration. It is consequently suggested that Yuldahansotang may attenuate the kainic acid-induced neuronal degeneration and increase the immunoreactivity of hippocampus in mouse.

• Korean Journal of Microbiology
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• v.54 no.4
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• pp.343-353
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• 2018

Our previous research demonstrated the essential role of the xenB gene in stress response to RDX by using Pseudomonas sp. HK-6 xenB knockout. We have extended this work to examine the cellular responses and altered proteomic profiles of the HK-6 xenA knockout mutant under RDX stress. The xenA mutant degraded RDX about 2-fold more slowly and its growth and survival rates were several-fold lower than the wild-type HK-6 strain. SEM revealed more severe morphological damages on the surface of the xenA mutant cells under RDX stress. The wild-type cells expressed proportionally-increased two stress shock proteins, DnaK and GroEL from the initial incubation time point or the relatively low RDX concentrations, but slightly less expressed at prolonged incubation period or higher RDX. However the xenA mutant did not produced DnaK and GroEL as RDX concentrations were gradually increased. The wild-type cells well maintained transcription levels of dnaA and groEL under increased RDX stress while those in the xenA mutant were decreased and eventually disappeared. The altered proteome profiles of xenA mutant cells under RDX stress also observed so that the 27 down-regulated plus the 3 up-regulated expression proteins were detected in 2-DE PAGE. These all results indicated that the intact xenA gene is necessary for maintaining cell integrity under the xenobiotic stress as well as performing an efficient RDX degradation process.

• The Journal of Korean Medicine
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• v.25 no.2
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• pp.67-76
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• 2004

Objectives : This study was designed to investigate the protective mechanisms of Palmul-tang on hypoxia-induced cytotoxicity in H9c2 cardiomyoblast cells. Methods : In this study, we used H9c2 cells. Cells were subjected to hypoxia in the absence and presence of $1000\mu\textrm{g}/ml$ Palmul-tang for 24 hrs. Cells were treated with various concentrations of Palmul-tang for 24 hrs. Cell viability was measured by MTT assay. Hypoxia markedly decreased the viability of H9c2 cells, which was characterized with apparent apoptotic features such as chromatin condensation as well as fragmentation of genomic DNA and nuclei. Results : Palmul-tang significantly reduced hypoxia-induced cell death and apoptotic characteristics. Also, Palmul-tang prevented mitochondrial dysfunction including the disruption of mitochondrial membrane permeability transition (MPT) and an increase in expression of apoptogenic Bcl-2 proteins in hypoxia-H9c2 cells. Conclusions; This study suggests that the protective effects of Palmul-tang against hypoxic damages may be mediated by the modulation of Bcl-2, Bax expression.

• Environmental Analysis Health and Toxicology
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• v.18 no.1
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• pp.15-19
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• 2003

Metallothionein gene expression activity of cadmium was investigated in a human lung epithelial cell line. Cells, grown to near confluence, were exposed to 0∼10 ${\mu}$M Cd metal for 6 hours. Cadmium did not cause morphological alteration in lung epithelial cells that are characteristic of cell damages such as cell shrinkage, detachment of the cell from its neighbors, cytoplasmic and chromatic condensation. However, metallothionein genes of MT-1 and MT-2 were rapidly induced in the treated cell measured by RT-PCR. Regarding the induction pattern of motallothionein mRNA, MT-1 mRNA was induced in a dependent manner. MT-2 mRNA induction, which was measured using oligo primers based on cDNA of human reticulocytes, seemed to be slightly increased in low doses but decreased at high concentration used in the experiment.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.93-94
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• 2001

Former studies dealing with combined effects caused by chemical compounds in the metabolically competent hepatoma cell line Hep G2 indicated that Hep G2 cells are useful and sensitive indicators for the identification of synergisms of promutagens, comutagens and antimutagens which are relevant in eukryontic (human) cells. In the present study we examined the modulation of DNA damages by the suspected antimutagens ascorbic acid, beta-carotene, alpha-naphthoflavone and beta-naphthoflavone in Hep G2 cells.(omitted)

• Korean Journal of Environmental Biology
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• v.23 no.3 s.59
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• pp.275-280
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• 2005

Development of the fourth-instar larvae of Chironomus riparius has a sensitive to ecdysteroid hormones. The 2D/E gel analysis for polypeptide expression reflecting early-ecdysterone inducible gene has conducted the emerged female from larval phase exposure to bisphenol A (BPA). In the 2D/E gel 1108 protein spots were identified. The visualized protein spots allowed extraction of 17 protein spots differed more than 3 fold in BPA treated animals, which was approximately $1.6\%$ of the total protein spots. However, polypeptide expression reflecting early-ecdysterone inducible gene didn't change after treatments. In addition, detection for the damages or changes in mitogenome level was observed. The conserved cytochrome oxidase I in DNA level affected exposure to BPA $(1{\mu}gL^{-1})$ in this preliminary study.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.133-133
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• 2003

In recent years. attention has focused on the application of the alkaline single cell gel electrophoresis (SCGE or Comet) assay in environmental mutagenesis. To evaluate the suitability of the assay as a monitoring. technique, the DNA damages in liver cells and erythrocytes of carp (Cyprinus carpio) exposed to benzo[${\alpha}$]pyrene (B[${\alpha}$]P) were estimated comparatively with the in vivo Comet assay and the micronucleus test (MNT).(omitted)

• Biomedical Science Letters
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• v.27 no.3
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• pp.111-120
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• 2021

Asbestos products had been widely used until 2007 in Korea since the 1930s. A total ban on their production and applications has been imposed because of the toxic effect of asbestos fibers on the human health. The inhaled asbestos fibers increase reactive oxygen species and inflammatory reactions in the respiratory airway including the alveolar sac, resulting in DNA damages and secretion of several inflammatory cytokines or chemokines. These paracrine communications promote the proliferation of fibroblasts and the synthesis of collagen fibers, thereby depositing them into the extracellular matrix at the interstitial space of alveoli. The fibrotic tissue hindered the gas exchange in the alveolus. This reviews describes not only the cytotoxic effects of asbestos fibers with different physical or chemical characteristics but also the interaction of cells that make up the respiratory airway to understand the molecular or cellular mechanisms of asbestos fiber-induced toxicity. In addition, we propose a pulmonary toxicity research technique based on the mini-lung that can mimic human respiratory system as an alternative to overcome the limitations of the conventional risk assessment of asbestos fibers.

• Journal of fish pathology
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• v.35 no.2
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• pp.177-183
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• 2022

We described Trichodina hokkaidoensis Mizuno, Matsuda, Nishikawa and Ito, 2022 from olive flounder Paralichthys olivaceus by morphological observation and molecular analysis. Morphological parameters of our specimen from 4 different sampling sites (Gangneung, Jeju, Wando, Taean) mostly coincided with those of T. hokkaidoensis. Some morphometric parameters of this trichodinid showed some inconsistency, depending on the sampling locations, but all of their partial small subunit ribosomal DNA sequences (1,182 bp) showed 100% homology with T. hokkaidoensis, originally described from artificially reared juvenile barfin flounder Verasper moseri from Japan. T. hokkaidoensis is known to cause epidermal damages to the host fish. However, there was no considerable pathological lesions in the olive flounder harboring T. hokkaidoensis in this study. The pathogenicity of T. hokkaidoensis against olive flounder needs to be investigated.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1733-1739
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• 2004

The water extract of Hwangryunhaedog-tang(HRHDT} has been traditionally used for treatment of ischemic heart and brain damage in oriental medicine. However, little is known about the mechanism by which the water extract of HRHDT rescues cells from these damages. This study was designed to investigate the protective mechanisms of HRHDT on hypoxia-induced cytotoxicity in H9c2 cardiomyoblast cells. Hypoxia, markedly decreased the viability of H9c2 cells, which was characterized with apparent apoptptic features such as chromatin condensation as well as fragmentation of genomic DNA and nuclei. However, HRHDT significantly reduced hypoxia-induced cell death and apoptotic characteristics. Also, HRHDT prevented the mitochondrial dysfunction including the disruption of mitochondria membrane permeability transition (MPT) and an increase in expression of anti-apoptotic Bcl-2 proteins in hypoxia-H9c2 cells. Taken together, this study suggests that the protective effects of the water extract of HRHDT against hypoxic damages may be mediated by the modulation of Bcl-2 and Bak expression.