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Molecular & cellular toxicology 15건

  1. [국내논문]   Cytotoxicity by Lead-induced nNOS Phosphorylation in a Dopaminergic CATH.a Cells: Roles of Protein Kinase A  

    Kwon, Yong-Hyun (Department of Pharmacology, Center for Advanced Medical Education, Inha University College of Medicine by BK-21 Project ) , Choi, Ji-Young (Department of Pharmacology, Center for Advanced Medical Education, Inha University College of Medicine by BK-21 Project ) , Shin, Mi-Kyung (Department of Pharmacology, Center for Advanced Medical Education, Inha University College of Medicine by BK-21 Project ) , Lim, Woo-Sung (Department of Urology, Inha University College of Medicine ) , Lee, Sung-Keun (Department of Pharmacology, Center for Advanced Medical Education, Inha University College of Medicine by BK-21 Project ) , Kang, Ju-Hee (Department of Pharmacology, Center for Advanced Medical Education, Inha University College of Medicine by BK-21 Project ) , Park, Chang-Shin (Department of Pharmacology, Center for Advanced Medical Education, Inha University College of Medicine by BK-21 Project)
    Molecular & cellular toxicology v.3 no.4 ,pp. 215 - 221 , 2007 , 1738-642x ,

    초록

    Neuronal cell toxicity induced by decreased nitric oxide (NO) production may be caused by modulation of constitutive neuronal NO synthase (nNOS). We used lead acetate ( $Pb^{2+}$ ) to modulate physiological NO release and the related pathways of protein kinases like PKC, CaM-KII, and PKA in CATH.a cells, a dopaminergic cell line that has constitutive nNOS activity. In the cells treated with $Pb^{2+}$ , cell viability and modulation (phosphorylation) levels of nNOS were determined by MTT assay and Western blot analysis, respectively. nNOS reductase activity (cytochrome c) was also assessed to compare the phosphorylation site-specific nNOS activity. nNOS activity was also determined by NADPH consumption rates. $Pb^{2+}$ treatment alone increased the phosphorylation of nNOS with decreased reductase activity. The phosphorylation levels increased markedly with decreased nNOS reductase activity, when $Pb^{2+}$ was combined with inhibitors for two (PKC and CaM-KII) or three (PKA, PKC and CaM-KII) protein kinases. Interestingly, when the cells were exposed to $Pb^{2+}$ plus PKC or CaM-KII inhibitor, the nNOS was phosphorylated strongly with the lowest activity. However, the levels of phosphorylated nNOS following $Pb^{2+}$ treatment decreased significantly after combined treatment with the PKA inhibitor, and $Pb^{2+}$ -induced suppression of reductase activity did not occur. These results demonstrate that physiological NO release in the neuronal cells exposed to $Pb^{2+}$ can be decreased by PKA-mediated nNOS phosphorylation that may be caused by interactions with PKC and/or CaM-KII.

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  2. [국내논문]   Gene Expression Profiling of Human Bronchial Epithelial (BEAS-2B) Cells Treated with Nitrofurantoin, a Pulmonary Toxicant   피인용횟수: 2

    Kim, Youn-Jung (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science and Technology ) , Song, Mee (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science and Technology ) , Ryu, Jae-Chun (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science and Technology)
    Molecular & cellular toxicology v.3 no.4 ,pp. 222 - 230 , 2007 , 1738-642x ,

    초록

    Some drugs may be limited in their clinical application due to their propensity towards their adverse effects. Toxicogenomic technology represents a useful approach for evaluating the toxic properties of new drug candidates early in the drug discovery process. Nitrofurantoin (NF) is clinical chemotherapeutic agent and antimicrobial and used to treatment of urinary tract infections. However, NF has been shown to result in pulmonary toxic effects. In this research, we revealed the changing expression gene profiles in BEAS-2B, human bronchial epithelial cell line, exposed to NF by using human oligonucleotide chip. Through the clustering analysis of gene expression profiles, we identified 136 up-regulated genes and 379 down-regulated genes changed by more than 2-fold by NF. This study identifies several interesting targets and functions in relation to NF-induced toxicity through a gene ontology analysis method including biological process, cellular components, molecular function and KEGG pathway.

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  3. [국내논문]   Toxicogenomic Study to Identify Potential New Mechanistic Markers on Direct-Acting Mutagens in Human Hepatocytes (THLE-3)  

    Kim, Youn-Jung (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science & Technology ) , Song, Mi-Kyung (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science & Technology ) , Song, Mee (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science & Technology ) , Ryu, Jae-Chun (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science & Technology)
    Molecular & cellular toxicology v.3 no.4 ,pp. 231 - 237 , 2007 , 1738-642x ,

    초록

    Exposure to DNA-damaging agents can elicit a variety of stress-related responses that may alter the expression of genes associated with numerous biological pathways. We used 19 k whole human genome chip to detect gene expression profiles and potential signature genes in human normal hepatocytes (THLE-3) by treatment of five direct acting mutagens, furylfuramide (AF-2), N-nitroso-N-methylurea (MNU), methylmethanesulfonate (MMS), 4-nitroquinoline-N-oxide (4-NQO) and 2-nitrofluorene (2NF) of the $IC_{20}$ concentration for 3 h. Fifty one up-regulated common genes and 45 down-regulated common genes above 1.5-fold by five direct-acting mutagens were identified by clustering analysis. Many of these changed genes have some association with apoptosis, control of cell cycle, regulation of transcription and signal transduction. Genes related to these functions, as TP73L, E2F5, MST016, SOX5, MAFB, LIF, SII3, TFIIS, EMR1, CYTL1, CX3CR1 and RHOH are up-regulated. Down-regulated genes are ALOX15B, xs155, IFITM1, BATF, VAV2, CD79A, DCDC2, TNFSF8 and KOX8. We suggest that gene expression profiling on mutagens by toxicogenomic analysis affords promising opportunities to reveal potential new mechanistic markers of genotoxicity.

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  4. [국내논문]   Proteomic Analysis of Differentially Expressed Proteins in Human Lung Cells Following Formaldehyde Treatment   피인용횟수: 3

    Jeon, Yu-Mi (Department of Biotechnology, SoonChunHyang University ) , Ryu, Jae-Chun (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science and Technology ) , Lee, Mi-Young (Department of Biotechnology, SoonChunHyang University)
    Molecular & cellular toxicology v.3 no.4 ,pp. 238 - 245 , 2007 , 1738-642x ,

    초록

    Chronic formaldehyde inhalation studies have suggested its relativity to teratogenicity, cancer incidence, neurodegenerative and vascular disorders. Many toxicological data on the formaldehyde toxicity are available, but proteomic results showing complete protein profiles are limited. Therefore, alterations of protein expression patterns upon formaldehyde treatment were investigated in the human lung epithelial cell line. Differentially expressed proteins following formaldehyde treatment were analyzed on 2-dimensional gels, and further analyzed by MALDI-TOF to identify the proteins. Among the identified proteins, 24 proteins were notably up-regulated and 6 proteins were down-regulated. In particular, cytoskeleton related protein named vinculin and Rho GDP dissociation inhibitor which plays a key role in apoptosis increased remarkably.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  5. [국내논문]   Identification of Marker Genes Related to Cardiovascular Toxicity of Doxorubicin and Daunorubicin in Human Umbilical Vein Endothelial Cells (HUVECs)   피인용횟수: 2

    Kim, Youn-Jung (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science & Technology ) , Lee, Ha-Eun (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science & Technology ) , Ryu, Jae-Chun (Cellular and Molecular Toxicology Laboratory, Korea Institute of Science & Technology)
    Molecular & cellular toxicology v.3 no.4 ,pp. 246 - 253 , 2007 , 1738-642x ,

    초록

    Doxorubicin and daunorubicin are excellent chemotherapeutic agents utilized for several types of cancer but the irreversible cardiac damage is the major limitation for its use. The biochemical mechanisms of doxorubicin- and daunorubicin- induced cardiotoxicity remain unclear. There are many reports on toxicity of doxorubicin and doxorubicin in cardiomyocytes, but effects in cardiovascular system by these drugs are almost not reported. In this study, we investigated gene expression profiles in human umbilical vein endothelial cells (HUVECs) to better understand the causes of doxorubicin and doxorubicininduced cardiovascular toxicity and to identify differentially expressed genes (DEGs). Through the clustering analysis of gene expression profiles, we identified 124 up-regulated common genes and 298 down-regulated common genes changed by more than 1.5-fold by all two cardiac toxicants. HUVECs responded to doxorubicin and doxorubicin damage by increasing levels of apoptosis, oxidative stress, EGF and lipid metabolism related genes. By clustering analysis, we identified some genes as potential markers on apoptosis effects of doxorubicin and doxorubicin. Six genes of these, BBC3, APLP1, FAS, TP53INP, BIRC5 and DAPK were the most significantly affected by doxorubicin and doxorubicin. Thus, this study suggests that these differentially expressed genes may play an important role in the cardiovascular toxic effects and have significant potential as novel biomarkers to doxorubicin and doxorubicin exposure.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  6. [국내논문]   The Anti-Inflammatory Effect of IH-901 in HT-29 Cells   피인용횟수: 1

    Lee, Seung-Min (Department of Biochemistry & Molecular biology, Korea University Medical College ) , Kim, Ki-Nam (Department of Biochemistry & Molecular biology, Korea University Medical College ) , Kim, Yu-Ri (Department of Biochemistry & Molecular biology, Korea University Medical College ) , Kim, Hye-Won (Department of Biochemistry & Molecular biology, Korea University Medical College ) , Shim, Boo-Im (Department of Biochemistry & Molecular biology, Korea University Medical College ) , Lee, Seung-Ho (Department of Biochemistry & Molecular biology, Korea University Medical College ) , Bae, Hak-Soon (Department of Biochemistry & Molecular biology, Korea University Medical College ) , Kim, In-Kyoung (Department of Biochemistry & Molecular biology, Korea University Medical College ) , Kim, Meyoung-Kon (Department of Biochemistry & Molecular biology, Korea University Medical College)
    Molecular & cellular toxicology v.3 no.4 ,pp. 254 - 261 , 2007 , 1738-642x ,

    초록

    20-O-( $\beta$ -D-Glucopyranosyl)-20 (S)-protopanaxadiol (IH-901) is one of the major metabolites of ginsenosides from Panax ginseng, and is suggested that IH-901 has been associated with various pharmacological and physiological activities. In this study, we demonstrate that IH-901 induced anti-inflammation in HT-29 human colon adenocarcinoma cells. Our results showed that IH-901 inhibited cell proliferation of HT-29 in a time- and dose-dependent manner. We also found that IH-901 was significantly decreased expression of iNOS compared with non-treated. We observed effect of IH-901 related with inflammatory genes using by cDNA microarray. We were known that the 34 inflammatory genes such as E2F, CDK6, TNF- $\alpha$ , and PKC were down-regulated. Thus, these results suggest that IH-901 may have a potential preventive factor to improving cancer induced by chronic inflammation.

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  7. [국내논문]   Somatic Mutations of the ENPP2 (Autotaxin/lysoPLD) Gene in Breast Cancer  

    Song, Jae-Hwi (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Kim, Jeong-Kyu (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Noh, Ji-Heon (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Jung, Kwang-Hwa (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Eun, Jung-Woo (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Kim, Chang-Jae (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Bae, Hyun-Jin (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Xie, Hong-Jian (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Ahn, Young-Min (Department of Kidney System, College of Oriental Medicine, Kyung Hee University ) , Lee, Sug-Hyung (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Yoo, Nam-Jin (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Lee, Jung-Young (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Park, Won-Sang (Lab of Pathology, College of Medicine, The Catholic University of Korea ) , Nam, Suk-Woo (Lab of Pathology, College of M)
    Molecular & cellular toxicology v.3 no.4 ,pp. 262 - 266 , 2007 , 1738-642x ,

    초록

    ENPP2, a 125 kDa secreted lysophopholipase D which originally identified as a tumor-motogen, Autotaxin, enhances cellular locomotion, cell proliferation, angiogenesis and cell survival by generating the signal molecule lysophosphatic acid or sphingosine-1-phosphate. Previous studies have suggested that expression of Autotaxin is associated with invasive phenotype in advanced breast carcinomas. Thus, to determine whether genetic alterations of ENPP2 gene are involved in the development or progression of breast cancer, we analyzed its somatic mutation in 85 breast carcinomas by single-stranded conformational polymorphism and sequencing. Overall, six ENPP2 mutations were found (7.0%), comprising five missense and one nonsense mutation (s). To our knowledge, this is the first report on ENPP2 mutation in breast carcinoma, and the data indicate that ENPP2 is occasionally mutated in breast carcinomas, and suggest that ENPP2 mutation may contribute to the tumor development in some breast carcinomas.

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  8. [국내논문]   Molecular Parameters for Assessing Marine Biotoxicity: Gene Expressions of Rockfish (Sebastes schlegeli) Exposed to Polycyclic Aromatic Hydrocarbons   피인용횟수: 1

    Woo, Seon-Ock (Southern Coastal Environment Research Division, Korea Ocean Research and Development Institute ) , Yum, Seung-Shic (Southern Coastal Environment Research Division, Korea Ocean Research and Development Institute ) , Park, Hong-Seog (Genome Research Center, Korea Research Institute of Bioscience and Technology ) , Jung, Jee-Hyun (Southern Coastal Environment Research Division, Korea Ocean Research and Development Institute ) , Lee, Suk-Chan (Department of Genetic Engineering, Sungkyunkwan University ) , Kim, So-Jung (Gyeongbuk Institute for Marine Bioindustry ) , Lee, Taek-Kyun (Southern Coastal Environment Research Division, Korea Ocean Research and Development Institute)
    Molecular & cellular toxicology v.3 no.4 ,pp. 267 - 272 , 2007 , 1738-642x ,

    초록

    Environmental and anthropogenic changes affect the health and stability of marine ecosystem. In this study we aimed to identify molecular biomarkers for ecotoxicological pollutants risk assessment in the rockfish (Sebastes schlegeli). We designed primers based on conserved sequences by multiple alignments of target genes from related species, and cloned the partial cDNAs of cytochrome P450 (CYP1A1), glutathione S-transferase (GST), metallothionein (MT), superoxide dismutase (SOD), ubiquitin (UB), vitellogenin (VTG) and $\beta$ -actin by reverse transcription polymerase chain reaction (RT-PCR) from S. schlegeli. Northern blot results indicated that these six genes expressions were significantly induced by benzo[a]pyrene (BaP, 1 ${\mu}M$ ) and that the level of each of their transcripts increased in BaP-exposed rockfish in a time-dependent manner. This study suggests that transcriptional changes in these six genes may be used for monitoring environmental exposure to polycyclic aromatic hydrocarbons (PAHs).

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  9. [국내논문]   N-oleoyl-D-erythro-sphingosine-based Analysis of Ceramide by High Performance Liquid Chromatography and Its Application to Determination in Diverse Biological Samples   피인용횟수: 1

    Lee, Youn-Sun (College of Pharmacy and CBITRC, Chungbuk National University ) , Choi, Heon-Kyo (College of Pharmacy and CBITRC, Chungbuk National University ) , Yoo, Jae-Myung (College of Pharmacy and CBITRC, Chungbuk National University ) , Choi, Kyong-Mi (College of Pharmacy and CBITRC, Chungbuk National University ) , Lee, Yong-Moon (College of Pharmacy and CBITRC, Chungbuk National University ) , Oh, Sei-Kwan (Department of Neuroscience, College of Medicine, Ewha Womans University ) , Kim, Tack-Joong (College of Pharmacy and CBITRC, Chungbuk National University ) , Yun, Yeo-Pyo (College of Pharmacy and CBITRC, Chungbuk National University ) , Hong, Jin-Tae (College of Pharmacy and CBITRC, Chungbuk National University ) , Okino, Nozomu (Department of Bioscience and Biotechnology, Graduate School of Bioresource and Bioenvironmental Sciences, Kyushu University ) , Ito, Makoto (Department of Bioscience and Biotechnology, Graduate School of Bioresource and Bioenvironmental Sciences, Kyushu University ) , Yoo, Hwan-Soo (College of Pharmacy and CBITRC, Chungbuk National University)
    Molecular & cellular toxicology v.3 no.4 ,pp. 273 - 281 , 2007 , 1738-642x ,

    초록

    Ceramide is involved in cell death as a lipid mediator of stress responses. In this study, we developed an improved method of ceramide quantification based on added synthetic ceramide and thin layer chromatography (TLC) separation, and applied to biological samples. Lipids were extracted from samples spiked with N-oleoyl-D-erythro-sphingosine ( $C_{17}$ ceramide) as an internal standard. Ceramide was resolved by TLC, complexed with fatty-acidfree bovine serum albumin (BSA), and deacylated by ceramidase (CDase). The released sphingosine was derivatized with o-phthalaldehyde (OPA) and measured by high performance liquid chromatography (HPLC). The limit of detection for ceramide was about 1-2 pmol and the lower limit of quantification was 5 pmol. Ceramide recovery was approximately 86-93%. Ceramide concentrations were determined in biological samples including cultured cells, mouse tissues, and mouse and human plasma. TLC separation of ceramide provides HPLC chromatogram with a clean background without any interfering peaks and the enhanced solubility of ceramide by BSAceramide complex leads to the increased deacylation of ceramide. The use of an internal standard for the determination of ceramide concentration in these samples provides an accurate and reproducible analytical method, and this method can be applicable to diverse biological samples.

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  10. [국내논문]   Effects of Olanzapine on Gene Expression Changes in MK-801-induced Neurotoxicity Using a High-density DNA Microarray  

    Jo, Jae-Hoon (College of Pharmacy, Chungnam National University ) , Kim, Seung-Jun (Genocheck Co. Ltd. ) , Yeon, Jong-Pil (Genocheck Co. Ltd. ) , Oh, Moon-Ju (Genocheck Co. Ltd. ) , Seo, Hye-Myung (Division of Molecular & Life Sciences, Hanyang University ) , Hwang, Seung-Yong (Genocheck Co. Ltd. ) , Kim, Sang-Kyum (College of Pharmacy, Chungnam National University ) , Kim, Bong-Hee (College of Pharmacy, Chungnam National University)
    Molecular & cellular toxicology v.3 no.4 ,pp. 282 - 291 , 2007 , 1738-642x ,

    초록

    Although the etiology of schizophrenia is known to be linked with the disturbance of glutamatergic and dopaminergic neurotransmission, little is known about the relationship between gene expression and the disease process. To identify genes related to abnormalities in glutamatergic and dopaminergic function, we investigated the effects of olanzapine in the changes of mRNA levels in the animal model of schizophrenia, using a high-density DNA microarray. Olanzapine (3.0 mg/kg, i.p.) significantly reduced hyperlocomotive activities, which was induced by MK-801 (1.0 mg/kg, i.p.). We identified that the expression of 719 genes were significantly altered more than two folds in the prefrontal cortex of the rats treated with MK-801. We selected 15 genes out of them by the changes of the expression pattern in the treatment of Olanzapine and/or MK801 for the further confirmation in RT-PCR. The administration of MK-801 increased the expression of 7 genes (NOS3, Hspb1, Hspa1a, CRH, Serpine1, Igfbp6, Snf1lk) and decreased the expression of 1 gene (Aldh1a2), which was attenuated by olanzapine. One gene (Prss12) was up-regulated after olanzapine treatment although it did not show the significant changes after MK-801 treatment. These results showed that antipsychotic drug, such as olanzapine, may alter the gene expression patterns, which were accompanied by MK-801-induced psychosis. Our results also provide us high-density DNA microarray technology could be potential approaches to find the candidate molecules for the therapeutics and also for the early diagnosis of psychiatric diseases.

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