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  1. Article ; Online: Lung developmental is altered after inhalation exposure to various concentrations of calcium arsenate.

    Chau, Binh / Witten, Mark L / Cromey, Doug / Chen, Yin / Lantz, R Clark

    Toxicology and applied pharmacology

    2021  Volume 432, Page(s) 115754

    Abstract: Exposure to dust from active and abandoned mining operations may be a very significant health hazard, especially to sensitive populations. We have previously reported that inhalation of real-world mine tailing dusts during lung development can alter lung ...

    Abstract Exposure to dust from active and abandoned mining operations may be a very significant health hazard, especially to sensitive populations. We have previously reported that inhalation of real-world mine tailing dusts during lung development can alter lung function and structure in adult male mice. These real-world dusts contain a mixture of metal(loid)s, including arsenic. To determine whether arsenic in inhaled dust plays a role in altering lung development, we exposed C57Bl/6 mice to a background dust (0 arsenic) or to the background dust containing either 3% or 10% by mass, calcium arsenate. Total level of exposure was kept at 100 μg/m
    MeSH term(s) Age Factors ; Airway Remodeling/drug effects ; Airway Resistance/drug effects ; Animals ; Arsenates/toxicity ; Bronchoconstriction/drug effects ; Calcium Compounds/toxicity ; Collagen/metabolism ; Down-Regulation ; Dust ; Female ; Gestational Age ; Inhalation Exposure ; Lung/drug effects ; Lung/growth & development ; Lung/metabolism ; Lung/pathology ; Male ; Mice, Inbred C57BL ; Pregnancy ; Prenatal Exposure Delayed Effects ; Uteroglobin/metabolism ; Mice
    Chemical Substances Arsenates ; Calcium Compounds ; Dust ; Scgb1a1 protein, mouse ; Collagen (9007-34-5) ; Uteroglobin (9060-09-7) ; calcium arsenate (95OX15I8ZU)
    Language English
    Publishing date 2021-10-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2021.115754
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  2. Article ; Online: Early life inhalation exposure to mine tailings dust affects lung development.

    Witten, Mark L / Chau, Binh / Sáez, Eduardo / Boitano, Scott / Clark Lantz, R

    Toxicology and applied pharmacology

    2019  Volume 365, Page(s) 124–132

    Abstract: Exposure to mine tailings dust from active and abandoned mining operations may be a very significant health hazard, especially to sensitive populations living in arid and semi-arid climates like the desert southwest of the US. It is anticipated that ... ...

    Abstract Exposure to mine tailings dust from active and abandoned mining operations may be a very significant health hazard, especially to sensitive populations living in arid and semi-arid climates like the desert southwest of the US. It is anticipated that early life exposures during sensitive times of development can lead to adult disease. However, very few studies have investigated the effects of inhalation exposure to real world dusts during lung development. Using a mouse model, we have examined the effect(s) of inhalation of real world mine tailing dusts under three separate conditions: (1) Exposure only during in utero development (exposure of the pregnant moms) (2) exposure only after birth and (3) exposures that occurred continuously during in utero development, through gestation and birth until the mice reached adulthood (28 days old). We found that the most significant changes in lung structure and function were observed in male mice when exposure occurred continuously throughout development. These changes included increased airway hyper-reactivity, increased expression of epithelial to mesenchymal (EMT) transition protein markers and increased expression of cytokines related to eosinophils. The data also indicate that in utero exposures through maternal inhalation can prime the lung of male mice for more severe responses to subsequent postnatal exposures. This may be due to epigenetic alterations in gene regulation, immune response, molecular signaling, and growth factors involved in lung development that may make the neonatal lung more susceptible to continued dust exposure.
    MeSH term(s) Age Factors ; Air Pollutants/toxicity ; Animals ; Bronchial Hyperreactivity/chemically induced ; Bronchial Hyperreactivity/physiopathology ; Cytokines/metabolism ; Dust ; Eosinophils/drug effects ; Eosinophils/metabolism ; Eosinophils/pathology ; Epithelial-Mesenchymal Transition/drug effects ; Female ; Gestational Age ; Inhalation Exposure/adverse effects ; Lung/drug effects ; Lung/metabolism ; Lung/pathology ; Lung/physiopathology ; Lung Diseases/chemically induced ; Lung Diseases/metabolism ; Lung Diseases/pathology ; Lung Diseases/physiopathology ; Male ; Mice, Inbred C57BL ; Mining ; Pregnancy ; Prenatal Exposure Delayed Effects ; Risk Assessment
    Chemical Substances Air Pollutants ; Cytokines ; Dust
    Language English
    Publishing date 2019-01-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2019.01.009
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  3. Article ; Online: DNA methylation of extracellular matrix remodeling genes in children exposed to arsenic.

    Gonzalez-Cortes, Tania / Recio-Vega, Rogelio / Lantz, Robert Clark / Chau, Binh T

    Toxicology and applied pharmacology

    2017  Volume 329, Page(s) 140–147

    Abstract: Several novel mechanistic findings regarding to arsenic's pathogenesis has been reported and some of them suggest that the etiology of some arsenic induced diseases are due in part to heritable changes to the genome via epigenetic processes such as DNA ... ...

    Abstract Several novel mechanistic findings regarding to arsenic's pathogenesis has been reported and some of them suggest that the etiology of some arsenic induced diseases are due in part to heritable changes to the genome via epigenetic processes such as DNA methylation, histone maintenance, and mRNA expression. Recently, we reported that arsenic exposure during in utero and early life was associated with impairment in the lung function and abnormal receptor for advanced glycation endproducts (RAGE), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) sputum levels. Based on our results and the reported arsenic impacts on DNA methylation, we designed this study in our cohort of children exposed in utero and early childhood to arsenic with the aim to associate DNA methylation of MMP9, TIMP1 and RAGE genes with its protein sputum levels and with urinary and toenail arsenic levels. The results disclosed hypermethylation in MMP9 promotor region in the most exposed children; and an increase in the RAGE sputum levels among children with the mid methylation level; there were also positive associations between MMP9 DNA methylation with arsenic toenail concentrations; RAGE DNA methylation with iAs, and %DMA; and finally between TIMP1 DNA methylation with the first arsenic methylation. A negative correlation between MMP9 sputum levels with its DNA methylation was registered. In conclusion, arsenic levels were positive associated with the DNA methylation of extracellular matrix remodeling genes;, which in turn could modifies the biological process in which they are involved causing or predisposing to lung diseases.
    MeSH term(s) Age Factors ; Arsenic/adverse effects ; Arsenic Poisoning/diagnosis ; Arsenic Poisoning/genetics ; Arsenic Poisoning/urine ; Child ; DNA Methylation/drug effects ; Extracellular Matrix/metabolism ; Female ; Genetic Markers ; Humans ; Male ; Maternal Exposure/adverse effects ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/metabolism ; Matrix Metalloproteinase 9/urine ; Nails/chemistry ; Pregnancy ; Prenatal Exposure Delayed Effects ; Promoter Regions, Genetic ; Receptor for Advanced Glycation End Products/genetics ; Receptor for Advanced Glycation End Products/metabolism ; Risk Assessment ; Sputum/chemistry ; Tissue Inhibitor of Metalloproteinase-1/genetics ; Tissue Inhibitor of Metalloproteinase-1/metabolism ; Tissue Inhibitor of Metalloproteinase-1/urine ; Water Pollutants, Chemical/adverse effects ; Water Supply
    Chemical Substances AGER protein, human ; Genetic Markers ; Receptor for Advanced Glycation End Products ; TIMP1 protein, human ; Tissue Inhibitor of Metalloproteinase-1 ; Water Pollutants, Chemical ; MMP9 protein, human (EC 3.4.24.35) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Arsenic (N712M78A8G)
    Language English
    Publishing date 2017-06-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2017.06.001
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  4. Article ; Online: Assessment of YAP gene polymorphisms and arsenic interaction in Mexican women with breast cancer.

    Michel-Ramirez, Gladis / Recio-Vega, Rogelio / Lantz, R Clark / Gandolfi, A Jay / Olivas-Calderon, Edgar / Chau, Binh T / Amistadi, Mary Kay

    Journal of applied toxicology : JAT

    2019  Volume 40, Issue 3, Page(s) 342–351

    Language English
    Publishing date 2019-10-21
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604625-3
    ISSN 1099-1263 ; 0260-437X
    ISSN (online) 1099-1263
    ISSN 0260-437X
    DOI 10.1002/jat.3907
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  5. Article ; Online: Linkages between Marketing Mix Components and Customer Satisfaction

    Bui Trung Thieu / Nguyen Vu Hoang / Pham Chau Binh / Nguyen Thi Le Huyen / Nguyen Thi Minh Hieu

    Journal of Economics and Business Research, Vol XXIII, Iss 1, Pp 123-

    An analysis on Google in Hanoi, Vietnam

    2017  Volume 148

    Abstract: Using SPSS and AMOS to conduct descriptive analysis and hypothetical analysis (t-test, one-way ANOVA and Regression), the study evaluates the importance of Marketing mix factors (4Ps) on Customer satisfaction of Google customers, using large-scale survey ...

    Abstract Using SPSS and AMOS to conduct descriptive analysis and hypothetical analysis (t-test, one-way ANOVA and Regression), the study evaluates the importance of Marketing mix factors (4Ps) on Customer satisfaction of Google customers, using large-scale survey inHanoi,Vietnamto generate primary data. Some “quotas” were built as quota sampling was used. Further, research implications, limitations and suggestions were mentioned respectively.
    Keywords Marketing mix ; Customer Satisfaction ; Google Inc ; Vietnam ; quota sampling ; Business ; HF5001-6182 ; Economic theory. Demography ; HB1-3840 ; Economics as a science ; HB71-74
    Language English
    Publishing date 2017-01-01T00:00:00Z
    Publisher Aurel Vlaicu University Editing House
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: Neonatal ontogeny of murine arylamine N-acetyltransferases: implications for arylamine genotoxicity.

    McQueen, Charlene A / Chau, Binh

    Toxicological sciences : an official journal of the Society of Toxicology

    2003  Volume 73, Issue 2, Page(s) 279–286

    Abstract: Age-related changes in the expression of xenobiotic biotransformation enzymes can result in differences in the rates of chemical activation and detoxification, affecting responses to the therapeutic and/or toxic effects of chemicals. Despite recognition ... ...

    Abstract Age-related changes in the expression of xenobiotic biotransformation enzymes can result in differences in the rates of chemical activation and detoxification, affecting responses to the therapeutic and/or toxic effects of chemicals. Despite recognition that children and adults may exhibit differences in susceptibility to chemicals, information about when in development specific biotransformation enzymes are expressed is incomplete. N-acetyltransferases (NATs) are phase II enzymes that catalyze the acetylation of arylamine and hydrazine carcinogens and therapeutic drugs. The postnatal expression of NAT1 and NAT2 was investigated in C57Bl/6 mice. Hepatic NAT1 and NAT2 messenger RNAs (mRNAs) increased with age from neonatal day (ND) 4 to adult in a nonlinear fashion. The presence of functional proteins was confirmed by measuring NAT activities with the isoform selective substrates p-aminobenzoic acid and isoniazid, as well as the carcinogens 2-aminofluorene and 4-aminobiphenyl (4ABP). Neonatal liver was able to acetylate all of the substrates, with activities increasing with age. Protein expression of CYP1A2, another enzyme involved in the biotransformation of arylamines, showed a similar pattern. The genotoxicity of 4ABP was assessed by determining hepatic 4ABP-DNA adducts. There was an age-dependent increase in 4ABP-DNA adducts during the neonatal period. Thus, developmental increases in expression of NAT1 and NAT2 genes in neonates are associated with less 4ABP genotoxicity. The age-related pattern of expression of biotransformation enzymes in mice is consistent with human data for NATs and suggests that this may play a role in developmental differences in arylamine toxicity.
    MeSH term(s) 4-Aminobenzoic Acid/pharmacokinetics ; 4-Aminobenzoic Acid/pharmacology ; Acetyltransferases ; Aging ; Amino Acid Transport System A ; Amino Acid Transport Systems ; Aminobiphenyl Compounds/pharmacokinetics ; Aminobiphenyl Compounds/toxicity ; Animals ; Animals, Newborn ; Arylamine N-Acetyltransferase ; Biotransformation ; Carrier Proteins/biosynthesis ; Carrier Proteins/genetics ; Cytochrome P-450 CYP1A2/biosynthesis ; DNA Adducts/analysis ; DNA Adducts/drug effects ; Fluorenes/pharmacokinetics ; Fluorenes/toxicity ; Isoenzymes ; Isoniazid/pharmacokinetics ; Isoniazid/pharmacology ; Liver/drug effects ; Liver/enzymology ; Mice ; Mice, Inbred C57BL ; Mutagens/pharmacokinetics ; Mutagens/toxicity ; RNA, Messenger/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
    Chemical Substances Amino Acid Transport System A ; Amino Acid Transport Systems ; Aminobiphenyl Compounds ; Carrier Proteins ; DNA Adducts ; Fluorenes ; Isoenzymes ; Mutagens ; RNA, Messenger ; Slc38a1 protein, mouse ; 4-biphenylamine (16054949HJ) ; 2-aminofluorene (3A69OS195N) ; Cytochrome P-450 CYP1A2 (EC 1.14.14.1) ; Acetyltransferases (EC 2.3.1.-) ; Arylamine N-Acetyltransferase (EC 2.3.1.5) ; N-acetyltransferase 1 (EC 2.3.1.5) ; 4-Aminobenzoic Acid (TL2TJE8QTX) ; Isoniazid (V83O1VOZ8L)
    Language English
    Publishing date 2003-06
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/kfg086
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  7. Article ; Online: Sulforaphane prevents pulmonary damage in response to inhaled arsenic by activating the Nrf2-defense response.

    Zheng, Yi / Tao, Shasha / Lian, Fangru / Chau, Binh T / Chen, Jie / Sun, Guifan / Fang, Deyu / Lantz, R Clark / Zhang, Donna D

    Toxicology and applied pharmacology

    2012  Volume 265, Issue 3, Page(s) 292–299

    Abstract: Exposure to arsenic is associated with an increased risk of lung disease. Novel strategies are needed to reduce the adverse health effects associated with arsenic exposure in the lung. Nrf2, a transcription factor that mediates an adaptive cellular ... ...

    Abstract Exposure to arsenic is associated with an increased risk of lung disease. Novel strategies are needed to reduce the adverse health effects associated with arsenic exposure in the lung. Nrf2, a transcription factor that mediates an adaptive cellular defense response, is effective in detoxifying environmental insults and prevents a broad spectrum of diseases induced by environmental exposure to harmful substances. In this report, we tested whether Nrf2 activation protects mice from arsenic-induced toxicity. We used an in vivo arsenic inhalation model that is highly relevant to low environmental human exposure to arsenic-containing dusts. Two-week exposure to arsenic-containing dust resulted in pathological alterations, oxidative DNA damage, and mild apoptotic cell death in the lung; all of which were blocked by sulforaphane (SF) in an Nrf2-dependent manner. Mechanistically, SF-mediated activation of Nrf2 alleviated inflammatory responses by modulating cytokine production. This study provides strong evidence that dietary intervention targeting Nrf2 activation is a feasible approach to reduce adverse health effects associated with arsenic exposure.
    MeSH term(s) Animals ; Arsenic/toxicity ; Bronchoalveolar Lavage Fluid/cytology ; Bronchoalveolar Lavage Fluid/immunology ; Cytokines/genetics ; Cytokines/immunology ; DNA Damage ; Immunohistochemistry ; Inhalation Exposure/adverse effects ; Isothiocyanates ; Lung Injury/chemically induced ; Lung Injury/immunology ; Lung Injury/prevention & control ; Mice ; Mice, Knockout ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/immunology ; RNA/chemistry ; RNA/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Thiocyanates/pharmacology
    Chemical Substances Cytokines ; Isothiocyanates ; NF-E2-Related Factor 2 ; Thiocyanates ; RNA (63231-63-0) ; sulforaphane (GA49J4310U) ; Arsenic (N712M78A8G)
    Language English
    Publishing date 2012-09-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2012.08.028
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  8. Article: Sulforaphane prevents pulmonary damage in response to inhaled arsenic by activating the Nrf2-defense response

    Zheng, Yi / Tao, Shasha / Lian, Fangru / Chau, Binh T / Chen, Jie / Sun, Guifan / Fang, Deyu / Lantz, R. Clark / Zhang, Donna D

    Toxicology and applied pharmacology. 2012 Dec. 15, v. 265, no. 3

    2012  

    Abstract: Exposure to arsenic is associated with an increased risk of lung disease. Novel strategies are needed to reduce the adverse health effects associated with arsenic exposure in the lung. Nrf2, a transcription factor that mediates an adaptive cellular ... ...

    Abstract Exposure to arsenic is associated with an increased risk of lung disease. Novel strategies are needed to reduce the adverse health effects associated with arsenic exposure in the lung. Nrf2, a transcription factor that mediates an adaptive cellular defense response, is effective in detoxifying environmental insults and prevents a broad spectrum of diseases induced by environmental exposure to harmful substances. In this report, we tested whether Nrf2 activation protects mice from arsenic-induced toxicity. We used an in vivo arsenic inhalation model that is highly relevant to low environmental human exposure to arsenic-containing dusts. Two-week exposure to arsenic-containing dust resulted in pathological alterations, oxidative DNA damage, and mild apoptotic cell death in the lung; all of which were blocked by sulforaphane (SF) in an Nrf2-dependent manner. Mechanistically, SF-mediated activation of Nrf2 alleviated inflammatory responses by modulating cytokine production. This study provides strong evidence that dietary intervention targeting Nrf2 activation is a feasible approach to reduce adverse health effects associated with arsenic exposure.
    Keywords DNA damage ; adverse effects ; apoptosis ; arsenic ; breathing ; cytokines ; environmental exposure ; humans ; inflammation ; mice ; models ; nutritional intervention ; risk ; toxicity ; transcription factors
    Language English
    Dates of publication 2012-1215
    Size p. 292-299.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2012.08.028
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  9. Article ; Online: In utero and postnatal exposure to arsenic alters pulmonary structure and function.

    Lantz, R Clark / Chau, Binh / Sarihan, Priyanka / Witten, Mark L / Pivniouk, Vadim I / Chen, Guan Jie

    Toxicology and applied pharmacology

    2008  Volume 235, Issue 1, Page(s) 105–113

    Abstract: In addition to cancer endpoints, arsenic exposures can also lead to non-cancerous chronic lung disease. Exposures during sensitive developmental time points can contribute to the adult disease. Using a mouse model, in utero and early postnatal exposures ... ...

    Abstract In addition to cancer endpoints, arsenic exposures can also lead to non-cancerous chronic lung disease. Exposures during sensitive developmental time points can contribute to the adult disease. Using a mouse model, in utero and early postnatal exposures to arsenic (100 ppb or less in drinking water) were found to alter airway reactivity to methacholine challenge in 28 day old pups. Removal of mice from arsenic exposure 28 days after birth did not reverse the alterations in sensitivity to methacholine. In addition, adult mice exposed to similar levels of arsenic in drinking water did not show alterations. Therefore, alterations in airway reactivity were irreversible and specific to exposures during lung development. These functional changes correlated with protein and gene expression changes as well as morphological structural changes around the airways. Arsenic increased the whole lung levels of smooth muscle actin in a dose dependent manner. The level of smooth muscle mass around airways was increased with arsenic exposure, especially around airways smaller than 100 microm in diameter. This increase in smooth muscle was associated with alterations in extracellular matrix (collagen, elastin) expression. This model system demonstrates that in utero and postnatal exposure to environmentally relevant levels of arsenic can irreversibly alter pulmonary structure and function in the adults.
    MeSH term(s) Aging ; Animals ; Animals, Newborn ; Arsenic/toxicity ; Collagen/metabolism ; Dose-Response Relationship, Drug ; Elastin/metabolism ; Female ; Gene Expression Regulation, Developmental/drug effects ; Lung/drug effects ; Lung/growth & development ; Lung/physiology ; Lung Diseases/chemically induced ; Lung Diseases/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth/drug effects ; Muscle, Smooth/pathology ; Muscle, Smooth/physiology ; Pregnancy ; Prenatal Exposure Delayed Effects
    Chemical Substances Collagen (9007-34-5) ; Elastin (9007-58-3) ; Arsenic (N712M78A8G)
    Language English
    Publishing date 2008-11-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2008.11.012
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  10. Article ; Online: Tanshinone I activates the Nrf2-dependent antioxidant response and protects against As(III)-induced lung inflammation in vitro and in vivo.

    Tao, Shasha / Zheng, Yi / Lau, Alexandria / Jaramillo, Melba C / Chau, Binh T / Lantz, R Clark / Wong, Pak K / Wondrak, Georg T / Zhang, Donna D

    Antioxidants & redox signaling

    2013  Volume 19, Issue 14, Page(s) 1647–1661

    Abstract: Aims: The NF-E2 p45-related factor 2 (Nrf2) signaling pathway regulates the cellular antioxidant response and activation of Nrf2 has recently been shown to limit tissue damage from exposure to environmental toxicants, including As(III). In an attempt to ...

    Abstract Aims: The NF-E2 p45-related factor 2 (Nrf2) signaling pathway regulates the cellular antioxidant response and activation of Nrf2 has recently been shown to limit tissue damage from exposure to environmental toxicants, including As(III). In an attempt to identify improved molecular agents for systemic protection against environmental insults, we have focused on the identification of novel medicinal plant-derived Nrf2 activators.
    Results: Tanshinones [tanshinone I (T-I), tanshinone IIA, dihydrotanshinone, cryptotanshinone], phenanthrenequinone-based redox therapeutics derived from the medicinal herb Salvia miltiorrhiza, have been tested as experimental therapeutics for Nrf2-dependent cytoprotection. Using a dual luciferase reporter assay overexpressing wild-type or mutant Kelch-like ECH-associated protein-1 (Keap1), we demonstrate that T-I is a potent Keap1-C151-dependent Nrf2 activator that stabilizes Nrf2 by hindering its ubiquitination. In human bronchial epithelial cells exposed to As(III), T-I displays pronounced cytoprotective activity with upregulation of Nrf2-orchestrated gene expression. In Nrf2 wild-type mice, systemic administration of T-I attenuates As(III) induced inflammatory lung damage, a protective effect not observed in Nrf2 knockout mice.
    Innovation: Tanshinones have been identified as a novel class of Nrf2-inducers for antioxidant tissue protection in an in vivo As(III) inhalation model, that is relevant to low doses of environmental exposure.
    Conclusion: T-I represents a prototype Nrf2-activator that displays cytoprotective activity upon systemic administration targeting lung damage originating from environmental insults. T-I based Nrf2-directed systemic intervention may provide therapeutic benefit in protecting other organs against environmental insults.
    MeSH term(s) Abietanes/therapeutic use ; Animals ; Antioxidants/therapeutic use ; Arsenic/toxicity ; Mice ; Mice, Knockout ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Phenanthrenes/therapeutic use ; Pneumonia/chemically induced ; Pneumonia/drug therapy ; Salvia miltiorrhiza/chemistry
    Chemical Substances Abietanes ; Antioxidants ; NF-E2-Related Factor 2 ; Phenanthrenes ; tanshinone (03UUH3J385) ; cryptotanshinone (5E9SXT166N) ; Arsenic (N712M78A8G)
    Language English
    Publishing date 2013-03-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2012.5117
    Database MEDical Literature Analysis and Retrieval System OnLINE

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