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Toxicology 9건

  1. [해외논문]   Editorial Board Members  


    Toxicology v.395 ,pp. IFC , 2018 , 0300-483x ,

    초록

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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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  2. [해외논문]   Editorial Board Members   SCI SCIE


    Toxicology v.395 ,pp. IFC - IFC , 2018 , 0300-483x ,

    초록

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    원문보기
    무료다운로드 유료다운로드

    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.

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

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  3. [해외논문]   Incorporating population-level genetic variability within laboratory models in toxicology: From the individual to the population   SCI SCIE

    Dornbos, Peter (Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI, USA ) , LaPres, John J. (Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI, USA)
    Toxicology v.395 ,pp. 1 - 8 , 2018 , 0300-483x ,

    초록

    Abstract Humans respond to chemical exposures differently due to many factors, such as previous and concurrent stressors, age, sex, and genetic background. The vast majority of laboratory-based toxicology studies, however, have not considered the impact of population-level variability within dose-response relationships. The lack of data dealing with the influence of genetic diversity on the response to chemical exposure provides a difficult challenge for risk assessment as individuals within the population will display a wide-range of responses following toxicant challenge. Notably, the genetic background of individuals plays a major role in the variability seen in a population-level response to a drug or chemical and, thus, there is growing interest in including genetic diversity into laboratory-models. Here we outline several laboratory-based models that can be used to assay the influence of genetic variability on an individual’s response to chemicals: 1) genetically-diverse cell lines, 2) human primary cells, 3) and genetically-diverse mouse panels. We also provide a succinct review for several seminal studies to highlight the capability, feasibility, and power of each of these models. This article is intended to highlight the need to include population-level genetic diversity into toxicological study designs via laboratory-based models with the goal to provide and supplement evidence in assessing the risk posed by chemicals to the human population. As such, incorporation of genetic variability will positively impact human-based risk assessment and provide empirical data to aid and influence decision-making processes in relation to chemical exposures.

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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.

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

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  4. [해외논문]   The 3-methyl-4-nitrophenol (PNMC) compromises airway epithelial barrier function   SCI SCIE

    An, Yun-Fang (Department of Otolaryngology, Head & Neck Surgery, The Second Hospital, Shanxi Medical University, Taiyuan, China ) , Geng, Xiao-Rui (The Research Center of Allergy & Immunology, Shenzhen University, Faculty of Medicine, Shenzhen, China ) , Mo, Li-Hua (The Research Center of Allergy & Immunology, Shenzhen University, Faculty of Medicine, Shenzhen, China ) , Liu, Jiang-Qi (The Research Center of Allergy & Immunology, Shenzhen University, Faculty of Medicine, Shenzhen, China ) , Yang, Li-Teng (Department of Respirology, The Third Affiliated Hospital, Shenzhen University, Shenzhen, China ) , Zhang, Xiao-Wen (Department of Otolaryngology, Head & Neck Surgery, The First Hospital, Guangzhou Medical University, Guangzhou, China ) , Liu, Zhi-Gang (The Research Center of Allergy & Immunology, Shenzhen University, Faculty of Medicine, Shenzhen, China ) , Zhao, Chang-Qing (Department of Otolaryngology, Head & Neck Surgery, The Second Hospital, Shanxi Medical University, Taiyuan, China ) , Yang, Ping-Chang (The Research Center of Allergy & Immunology, Shenzhen University, Faculty of Medicine, Shenzhen, China)
    Toxicology v.395 ,pp. 9 - 14 , 2018 , 0300-483x ,

    초록

    Abstract Background and aims It is recognized that the air pollution is associated with the pathogenesis of airway diseases. This study aims to elucidate the role of the 3-methyl-4-nitrophenol (PNMC), one of the components of diesel-exhaust particles, in compromising the airway epithelial barrier integrity. Methods A549 cells, an airway epithelial cell line, were cultured to monolayers to be used as an in vitro epithelial barrier model. BALB/c mice were treated with nasal drops containing PNMC to test the effects of PNMC on alternating the airway epithelial barrier functions. Results Exposure of mice to PNMC induced nasal epithelial cell apoptosis and increased the permeability of the nasal epithelial barrier. PNMC increased casp8 and casp3 activities in nasal epithelial cells. Exposure to PNMC up regulated Fas and FasL expression in airway epithelial cells. Inhibition of caspase abolished the PNMC-induced airway epithelial barrier dysfunction. Conclusion Exposure of airway mucosa to PNMC induces epithelial cell apoptosis and compromises the epithelial barrier function, which can be prevented by the inhibition of caspases. Highlights Exposure of mice to 4-nitro-m-cresol (PNMC) induced nasal epithelial cell apoptosis. Exposure of mice to PNMC increased the permeability of the nasal epithelial barrier. PNMC increased casp8 and casp3 activities in nasal epithelial cells. Exposure to PNMC up regulated Fas and FasL expression in airway epithelial cells. Inhibition of caspase abolished the PNMC-induced airway epithelial barrier dysfunction.

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

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  5. [해외논문]   PFE-360-induced LRRK2 inhibition induces reversible, non-adverse renal changes in rats   SCI SCIE

    Andersen, Michael Aagaard (Department of Neurodegeneration, Neuroscience Drug Discovery DK, H. Lundbeck A/S, Valby, Denmark ) , Wegener, Karen Malene (Department of Regulatory Toxicology & Safety Assessment, H. Lundbeck A/S, Valby, Denmark ) , Larsen, Steen (Department of Regulatory Toxicology & Safety Assessment, H. Lundbeck A/S, Valby, Denmark ) , Badolo, Lassina (Department of Discovery DMPK, H. Lundbeck A/S, Valby, Denmark ) , Smith, Garrick Paul (Department of Discovery Chemistry 2, H. Lundbeck A/S, Valby, Denmark ) , Jeggo, Ross (Department of Neurodegeneration, Neuroscience Drug Discovery DK, H. Lundbeck A/S, Valby, Denmark ) , Jensen, Poul Henning (Department of Biomedicine, Dandrite, Faculty of Health, Aarhus University, Aarhus, Denmark ) , Sotty, Florence (Department of Neurodegeneration, Neuroscience Drug Discovery DK, H. Lundbeck A/S, Valby, Denmark ) , Christensen, Kenneth Vielsted (Department of Neurodegeneration, Neuroscience Drug Discovery DK, H. Lundbeck A/S, Valby, Denmark ) , Thougaard, Annemette (Department of Exploratory Toxicology, Nonclinical Safety Research, H. Lundbeck A/S, Valby, Denmark)
    Toxicology v.395 ,pp. 15 - 22 , 2018 , 0300-483x ,

    초록

    Abstract Parkinson’s disease (PD) is a progressive neurodegenerative disorder for which there is no existing therapeutic approach to delay or stop progression. Genetic, biochemical and pre-clinical studies have provided evidence that leucine-rich-repeat-kinase-2 (LRRK2) kinase is involved in the pathogenesis of PD, and small molecule LRRK2 inhibitors represent a novel potential therapeutic approach. However, potentially adverse target-related effects have been discovered in the lung and kidneys of LRRK2 knock-out (ko) mice and rats. It is unclear if the LRRK2 ko effect in the kidneys and lung is also induced by pharmacological inhibition of the LRRK2 kinase. Here, we show that treatment with the LRRK2 inhibitor PFE-360 in rats induces a morphological kidney phenotype resembling that of the LRRK2 ko rats, whereas no effects were observed in the lung. The PFE-360 treatment induced morphological changes characterised by darkened kidneys and progressive accumulation of hyaline droplets in the renal proximal tubular epithelium. However, no histopathological evidence of renal tubular injury or changes in the blood and urine parameters that would be indicative of kidney toxicity or impaired kidney function were observed after up to 12 weeks of treatment. Morphological changes were detected in the kidney after 2 weeks of treatment and were partially reversible within a 30 day treatment-free period. Our findings suggest that pharmacological LRRK2 inhibition may not have adverse consequences for kidney function.

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

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  6. [해외논문]   In utero combined di-(2-ethylhexyl) phthalate and diethyl phthalate exposure cumulatively impairs rat fetal Leydig cell development   SCI SCIE

    Hu, Guoxin (Department of Pharmacology, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325000, China ) , Li, Junwei (Department of Pharmacology, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325000, China ) , Shan, Yuanyuan (Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan West Road, Wenzhou, Zhejiang 325027, China ) , Li, Xiaoheng (Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan West Road, Wenzhou, Zhejiang 325027, China ) , Zhu, Qiqi (Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan West Road, Wenzhou, Zhejiang 325027, China ) , Li, Huitao (Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan West Road, Wenzhou, Zhejiang 325027, China ) , Wang, Yiyan (Department of Anesthesiology, The Second) , Chen, Xiaofang , Lian, Qingquan , Ge, Ren-Shan
    Toxicology v.395 ,pp. 23 - 33 , 2018 , 0300-483x ,

    초록

    Abstract Phthalate diesters, including di-(2-ethylhexyl) phthalate (DEHP) and diethyl phthalate (DEP), are chemicals to which humans are ubiquitously exposed. Humans are exposed simultaneously to multiple environmental chemicals, including DEHP and DEP. There is little information available about how each chemical may interact to each other if they were exposed at same time. The present study investigated effects of the combinational exposure of rats to DEP and DEHP on fetal Leydig cell development. The results showed that the gestational (GD12-20) exposure of DEP + DEHP resulted in synergistic and/or dose-additive effects on the development of fetal Leydig cell. The lowest observed adverse-effect levels (LOAEL) for fetal Leydig cell (aggregation and cell size), and StAR expressions were of 10 mg/kg and, lower than when these chemicals were exposed alone. Also, mathematical modeling the response curves supports the dose-addition model over integrated-addition model. Overall, these data demonstrate that individual phthalate with a similar mechanism of action can elicit cumulative, dose additive, and sometimes synergistic, effects on the development of male reproductive system when administered as a mixture. Highlights Phthalates dose-dependently cause fetal Leydig cell aggregation. DEHP is more potent to inhibit testosterone production than DEP. DEP and DEHP can elicit dose addition effect on FLC development.

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  7. [해외논문]   Mechanisms of mitochondrial toxicity of the kinase inhibitors ponatinib, regorafenib and sorafenib in human hepatic HepG2 cells   SCI SCIE

    Paech, Franziska (Division of Clinical Pharmacology & Toxicology, University Hospital, Basel, Switzerland ) , Mingard, Cé (Division of Clinical Pharmacology & Toxicology, University Hospital, Basel, Switzerland ) , cile (Division of Clinical Pharmacology & Toxicology, University Hospital, Basel, Switzerland ) , Grü (Division of Clinical Pharmacology & Toxicology, University Hospital, Basel, Switzerland ) , nig, David (Division of Clinical Pharmacology & Toxicology, University Hospital, Basel, Switzerland ) , Abegg, Vanessa F. (Division of Clinical Pharmacology & Toxicology, University Hospital, Basel, Switzerland) , Bouitbir, Jamal , Krä , henbü , hl, Stephan
    Toxicology v.395 ,pp. 34 - 44 , 2018 , 0300-483x ,

    초록

    Abstract Previous studies have shown that certain kinase inhibitors are mitochondrial toxicants. In the current investigation, we determined the mechanisms of mitochondrial impairment by the kinase inhibitors ponatinib, regorafenib, and sorafenib in more detail. In HepG2 cells cultured in galactose and exposed for 24 h, all three kinase inhibitors investigated depleted the cellular ATP pools at lower concentrations than cytotoxicity occurred, compatible with mitochondrial toxicity. The kinase inhibitors impaired the activity of different complexes of the respiratory chain in HepG2 cells exposed to the toxicants for 24 h and in isolated mouse liver mitochondria exposed acutely. As a consequence, they increased mitochondrial production of ROS in HepG2 cells in a time- and concentration-dependent fashion and decreased the mitochondrial membrane potential concentration-dependently. In HepG2 cells exposed for 24 h, they induced mitochondrial fragmentation, lysosome content and mitophagy as well as mitochondrial release of cytochrome c, leading to apoptosis and/or necrosis. In conclusion, the kinase inhibitors ponatinib, regorafenib, and sorafenib impaired the function of the respiratory chain, which was associated with increased ROS production and a drop in the mitochondrial membrane potential. Despite activation of defense measures such as mitochondrial fission and mitophagy, some cells were liquidated concentration-dependently by apoptosis or necrosis. Mitochondrial dysfunction may represent a toxicological mechanism of hepatotoxicity associated with certain kinase inhibitors. Highlights Certain kinase inhibitors inhibit the respiratory chain of liver mitochondria. The mitochondrial membrane potential drops, causing fission and mitophagy. Despite these defense measures, some mitochondria burst and release cytochrome c. Cytochrome c in the cytoplasm causes apoptosis or necrosis depending on the ATP level.

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  8. [해외논문]   Nickel ions bind to HSP90β and enhance HIF-1α-mediated IL-8 expression   SCI SCIE

    Asakawa, Sanki (Laboratory of Pharmacotherapy of Life-Style Related Diseases, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan ) , Onodera, Ryo (Laboratory of Pharmacotherapy of Life-Style Related Diseases, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan ) , Kasai, Koji (Laboratory of Pharmacotherapy of Life-Style Related Diseases, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan ) , Kishimoto, Yu (Laboratory of Pharmacotherapy of Life-Style Related Diseases, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan ) , Sato, Taiki (Laboratory of Pharmacotherapy of Life-Style Related Diseases, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan ) , Segawa, Ryosuke (Laboratory of Pharmacotherapy of Life-Style Related Diseases, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan ) , Mizuno, Natsumi (Laboratory of Pharmacotherapy of Life-Style Related Diseases, Graduate School of Pharmaceutical Sciences,) , Ogasawara, Kouetsu , Moriya, Takahiro , Hiratsuka, Masahiro , Hirasawa, Noriyasu
    Toxicology v.395 ,pp. 45 - 53 , 2018 , 0300-483x ,

    초록

    Abstract Nickel ions (Ni 2+ ) eluted from biomedical devices cause inflammation and Ni allergy. Although Ni 2+ and Co 2+ elicit common effects, Ni 2+ induces a generally stronger inflammatory reaction. However, the molecular mechanism by which Ni 2+ and Co 2+ induce such different responses remains to be elucidated. In the present study, we compared the effects of Ni 2+ and Co 2+ on the expression of interleukin (IL)-8 in human monocyte THP-1 cells. We report that NiCl 2 but not CoCl 2 induced the expression of IL-8; in contrast, CoCl 2 elicited a higher expression of hypoxia-inducible factor-1α (HIF-1α). The NiCl 2 -induced expression of IL-8 in late phase was blocked by a HIF-1α inhibitor, PX-478, indicating that NiCl 2 targets additional factors responsible for activating HIF-1α. To identify such targets, proteins that bound preferentially to Ni-NTA beads were analyzed by LC/MS/MS. The analysis yielded heat shock protein 90β (HSP90β) as a possible candidate. Furthermore, Ni 2+ reduced the interaction of HSP90β with HIF-1α, and instead promoted the interaction between HIF-1α and HIF-1β, as well as the nuclear localization of HIF-1α. Using various deletion variants, we showed that Ni 2+ could bind to the linker domain on HSP90β. These results suggest that HSP90β plays important roles in Ni 2+ -induced production of IL-8 and could be a potential target for the regulation of Ni 2+ -induced inflammation.

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  9. [해외논문]   Differentially DNA methylation changes induced in vitro by traffic-derived nanoparticulate matter   SCI SCIE

    Lei, Xiaoning (State Environmental Protection Key Laboratory of Risk Assessment and Control on Chemical Processes, East China University of Science and Technology (ECUST), Shanghai, China ) , Muscat, Joshua E. (Department of Public Health Sciences, The Pennsylvania State University College of Medicine, Penn State Hershey Medical Center, Hershey, PA, United States ) , Zhang, Bo (Department of Biochemistry & Molecular Biology, The Pennsylvania State University College of Medicine, Penn State Hershey Medical Center, Hershey, PA, United States ) , Sha, Xuyang (Shanghai High School, Shanghai, China ) , Xiu, Guangli (State Environmental Protection Key Laboratory of Risk Assessment and Control on Chemical Processes, East China University of Science and Technology (ECUST), Shanghai, China)
    Toxicology v.395 ,pp. 54 - 62 , 2018 , 0300-483x ,

    초록

    Abstract The cytotoxicity, apoptosis, reactive oxygen species (ROS) and DNA damage induced by the commercial diesel exhaust particulate matter (PM) (SRM2975) with concentrations ranging from 0.1 μg mL −1 to 20 μg mL −1 were assessed in human umbilical vein endothelial cells (HUVECs) in vitro. An epigenetics-wide investigation of DNA methylation profiles was also performed using a new methylation beadchip (Illumina 850 K) to identify the health effects of traffic-derived nanoparticulate matter (nPM) with a concentration of 20 μg mL −1 . By characterising its physical and chemical properties, we found that SRM2975 is a highly disordered graphitic structure material with a nanometer dimension and a large surface area. Low levels of traffic-derived nPM (≤10 μg mL −1 ) induced cell apoptosis and DNA damage as well as increased intracellular ROS levels (p −1 (p Highlights Cytotoxicology, apoptosis, reactive oxygen species and DNA damage induced by traffic-derived nanoparticulate matter were assessed. The epigenetics-wide DNA methylation was investigated using a new Methylation Beadchip (Illumina 850 K). The majority of enriched Gene Ontology term are known as related to calcium ion and heart muscle. The top three Kyoto encyclopedia of genes and genomes enriched pathways are involved in three common subtypes of cardiomyopathy. Graphical abstract [DISPLAY OMISSION]

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