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Book ; Online ; E-Book: Arsenic

States, J. Christopher

exposure sources, health risks, and mechanisms of toxicity

2016

Author's details	edited by J. Christopher States
Keywords	Arbeitssicherheit u. Umweltschutz i. d. Chemie ; Chemical and Environmental Health and Safety ; Chemie ; Chemistry ; Environmental Toxicology ; Epidemiologie u. Biostatistik ; Epidemiology & Biostatistics ; Gesundheits- u. Sozialwesen ; Health & Social Care ; Umwelttoxikologie ; CH25: Umwelttoxikologie ; CH50: Arbeitssicherheit u. Umweltschutz i. d. Chemie ; HE55: Epidemiologie u. Biostatistik
Language	English
Size	1 Online-Ressource (xiv, 560 Seiten)
Publisher	Wiley
Publishing place	Hoboken, New Jersey
Publishing country	United States
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019003815
ISBN	978-1-118-87678-7 ; 9781118511145 ; 1-118-87678-4 ; 111851114X
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Invited Perspective: Humanized Mice for Arsenic Metabolism-A Better Model for Investigating Arsenic-Induced Diseases?

States, J Christopher / Barchowsky, Aaron

Environmental health perspectives

2023 Volume 131, Issue 12, Page(s) 121308

MeSH term(s)	Animals ; Mice ; Arsenic/toxicity ; Disease Models, Animal
Chemical Substances	Arsenic (N712M78A8G)
Language	English
Publishing date	2023-12-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	195189-0
ISSN	1552-9924 ; 0091-6765 ; 1078-0475
ISSN (online)	1552-9924
ISSN	0091-6765 ; 1078-0475
DOI	10.1289/EHP13932
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Article ; Online: 2020-2021 Toxicological Sciences Paper of the Year.

States, J Christopher / Peters, Jeffrey M

Toxicological sciences : an official journal of the Society of Toxicology

2022 Volume 186, Issue 2, Page(s) 177–178

Language	English
Publishing date	2022-05-04
Publishing country	United States
Document type	Editorial
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfac020
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Article ; Online: Chronic arsenic exposure induces malignant transformation of human HaCaT cells through both deterministic and stochastic changes in transcriptome expression.

Banerjee, Mayukh / Srivastava, Sudhir / Rai, Shesh N / States, J Christopher

Toxicology and applied pharmacology

2024 Volume 484, Page(s) 116865

Abstract: Biological processes are inherently stochastic, i.e., are partially driven by hard to predict random probabilistic processes. Carcinogenesis is driven both by stochastic and deterministic (predictable non-random) changes. However, very few studies ... ...

Abstract	Biological processes are inherently stochastic, i.e., are partially driven by hard to predict random probabilistic processes. Carcinogenesis is driven both by stochastic and deterministic (predictable non-random) changes. However, very few studies systematically examine the contribution of stochastic events leading to cancer development. In differential gene expression studies, the established data analysis paradigms incentivize expression changes that are uniformly different across the experimental versus control groups, introducing preferential inclusion of deterministic changes at the expense of stochastic processes that might also play a crucial role in the process of carcinogenesis. In this study, we applied simple computational techniques to quantify: (i) The impact of chronic arsenic (iAs) exposure as well as passaging time on stochastic gene expression and (ii) Which genes were expressed deterministically and which were expressed stochastically at each of the three stages of cancer development. Using biological coefficient of variation as an empirical measure of stochasticity we demonstrate that chronic iAs exposure consistently suppressed passaging related stochastic gene expression at multiple time points tested, selecting for a homogenous cell population that undergo transformation. Employing multiple balanced removal of outlier data, we show that chronic iAs exposure induced deterministic and stochastic changes in the expression of unique set of genes, that populate largely unique biological pathways. Together, our data unequivocally demonstrate that both deterministic and stochastic changes in transcriptome-wide expression are critical in driving biological processes, pathways and networks towards clonal selection, carcinogenesis, and tumor heterogeneity.
MeSH term(s)	Humans ; Arsenic/toxicity ; Transcriptome ; HaCaT Cells ; Stochastic Processes ; Cell Transformation, Neoplastic/chemically induced ; Cell Transformation, Neoplastic/genetics
Chemical Substances	Arsenic (N712M78A8G)
Language	English
Publishing date	2024-02-17
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.2024.116865
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Article ; Online: Chronic arsenic exposure suppresses proteasomal and autophagic protein degradation.

Augenstein, Isabell I / Nail, Alexandra N / Ferragut Cardoso, Ana P / States, J Christopher / Banerjee, Mayukh

Environmental toxicology and pharmacology

2024 Volume 107, Page(s) 104398

Abstract: Ubiquitin Proteasomal System (UPS) and autophagy dysregulation initiate cancer. These pathways are regulated by zinc finger proteins. Trivalent inorganic arsenic (iAs) displaces zinc from zinc finger proteins disrupting functions of important cellular ... ...

Abstract	Ubiquitin Proteasomal System (UPS) and autophagy dysregulation initiate cancer. These pathways are regulated by zinc finger proteins. Trivalent inorganic arsenic (iAs) displaces zinc from zinc finger proteins disrupting functions of important cellular proteins. The effect of chronic environmental iAs exposure (100 nM) on UPS has not been studied. We tested the hypothesis that environmental iAs exposure suppresses UPS, activating autophagy as a compensatory mechanism. We exposed skin (HaCaT and Ker-CT; independent quadruplicates) and lung (BEAS-2B; independent triplicates) cell cultures to 0 or 100 nM iAs for 7 or 8 weeks. We quantified ER stress (XBP1 splicing employing Reverse Transcriptase -Polymerase Chain Reaction), proteasomal degradation (immunoblots), and initiation and completion of autophagy (immunoblots). We demonstrate that chronic iAs exposure suppresses UPS, initiates autophagy, but suppresses autophagic protein degradation in skin and lung cell lines. Our data suggest that chronic iAs exposure inhibits autophagy which subsequently suppresses UPS.
MeSH term(s)	Arsenic/toxicity ; Proteolysis ; Arsenicals ; Proteasome Endopeptidase Complex ; Autophagy
Chemical Substances	Arsenic (N712M78A8G) ; Arsenicals ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2024-02-23
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1318302-3
ISSN	1872-7077 ; 1382-6689
ISSN (online)	1872-7077
ISSN	1382-6689
DOI	10.1016/j.etap.2024.104398
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Article ; Online: Zinc supplementation prevents arsenic-induced dysregulation of ZRANB2 splice function.

Bastick, Jonathan C / Banerjee, Mayukh / States, J Christopher

Environmental toxicology and pharmacology

2022 Volume 94, Page(s) 103921

Abstract: Environmentally relevant (100 nM) inorganic arsenic (iAs) exposure displaces zinc from zinc fingers of upstream splice regulator ZRANB2 disrupting the splicing of its target TRA2B. Excess zinc displaced iAs from ZRANB2 zinc fingers in cell free system. ... ...

Abstract	Environmentally relevant (100 nM) inorganic arsenic (iAs) exposure displaces zinc from zinc fingers of upstream splice regulator ZRANB2 disrupting the splicing of its target TRA2B. Excess zinc displaced iAs from ZRANB2 zinc fingers in cell free system. Thus, the hypothesis that zinc supplementation could prevent iAs-mediated disruption of ZRANB2 splice function in human keratinocytes was tested. The data show that zinc supplementation prevented iAs-induced dysregulation of TRA2B splicing by ZRANB2 as well as the induction of ZRANB2 protein expression. These results provide additional support for the hypothesis that zinc supplementation could prevent iAs-mediated disease in iAs-exposed populations.
MeSH term(s)	Arsenic/metabolism ; Arsenic/toxicity ; Dietary Supplements ; Humans ; RNA-Binding Proteins/metabolism ; Zinc/metabolism ; Zinc/pharmacology
Chemical Substances	RNA-Binding Proteins ; ZRANB2 protein, human ; Zinc (J41CSQ7QDS) ; Arsenic (N712M78A8G)
Language	English
Publishing date	2022-06-25
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1318302-3
ISSN	1872-7077 ; 1382-6689
ISSN (online)	1872-7077
ISSN	1382-6689
DOI	10.1016/j.etap.2022.103921
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Article ; Online: Zinc supplementation prevents mitotic accumulation in human keratinocyte cell lines upon environmentally relevant arsenic exposure.

Banerjee, Mayukh / Yaddanapudi, Kavitha / States, J Christopher

Toxicology and applied pharmacology

2022 Volume 454, Page(s) 116255

Abstract: Disrupted cell cycle progression underlies the molecular pathogenesis of multiple diseases. Chronic exposure to inorganic arsenic (iAs) is a global health issue leading to multi-organ cancerous and non-cancerous diseases. Exposure to supratherapeutic ... ...

Abstract	Disrupted cell cycle progression underlies the molecular pathogenesis of multiple diseases. Chronic exposure to inorganic arsenic (iAs) is a global health issue leading to multi-organ cancerous and non-cancerous diseases. Exposure to supratherapeutic concentrations of iAs causes cellular accumulation in G2 or M phase of the cell cycle in multiple cell lines by inducing cyclin B1 expression. It is not clear if iAs exposure at doses corresponding to serum levels of chronically exposed populations (∼100 nM) has any effect on cell cycle distribution. In the present study we investigated if environmentally relevant iAs exposure induced cell cycle disruption and mechanisms thereof employing two human keratinocyte cell lines (HaCaT and Ker-CT), flow cytometry, immunoblots and quantitative real-time PCR (qRT-PCR). iAs exposure (100 nM; 24 h) led to mitotic accumulation of cells in both cell lines, along with the stabilization of ANAPC11 ubiquitination targets cyclin B1 and securin, without affecting their steady state mRNA levels. This result suggested that induction of cyclin B1 and securin is modulated at the level of protein degradation. Moreover, zinc supplementation successfully prevented iAs-induced mitotic accumulation and stabilization of cyclin B1 and securin without affecting their mRNA levels. Together, these data suggest that environmentally relevant iAs exposure leads to mitotic accumulation possibly by displacing zinc from the RING finger subunit of anaphase promoting complex/cyclosome (ANAPC11), the cell cycle regulating E3 ubiquitin ligase. This early cell cycle disruptive effect of environmentally relevant iAs concentration could underpin the molecular pathogenesis of multiple diseases associated with chronic iAs exposure.
MeSH term(s)	Anaphase-Promoting Complex-Cyclosome ; Apc11 Subunit, Anaphase-Promoting Complex-Cyclosome ; Arsenic/toxicity ; Cell Line ; Cyclin B1/genetics ; Dietary Supplements ; Humans ; Keratinocytes ; RNA, Messenger ; Securin ; Ubiquitin-Protein Ligases ; Zinc
Chemical Substances	Cyclin B1 ; RNA, Messenger ; Securin ; Anaphase-Promoting Complex-Cyclosome (EC 2.3.2.27) ; Apc11 Subunit, Anaphase-Promoting Complex-Cyclosome (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Zinc (J41CSQ7QDS) ; Arsenic (N712M78A8G)
Language	English
Publishing date	2022-09-24
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.2022.116255
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Article ; Online: miRNAs and arsenic-induced carcinogenesis.

Nail, Alexandra N / Ferragut Cardoso, Ana P / Montero, Lakyn K / States, J Christopher

Advances in pharmacology (San Diego, Calif.)

2023 Volume 96, Page(s) 203–240

Abstract: Arsenic-induced carcinogenesis is a worldwide health problem. Identifying the molecular mechanisms responsible for the induction of arsenic-induced cancers is important for developing treatment strategies. MicroRNA (miRNA) dysregulation is known to ... ...

Abstract	Arsenic-induced carcinogenesis is a worldwide health problem. Identifying the molecular mechanisms responsible for the induction of arsenic-induced cancers is important for developing treatment strategies. MicroRNA (miRNA) dysregulation is known to affect development and progression of human cancer. Several studies have identified an association between altered miRNA expression in cancers from individuals chronically exposed to arsenic and in cell models for arsenic-induced carcinogenesis. This chapter provides a comprehensive review for miRNA dysregulation in arsenic-induced cancer.
MeSH term(s)	Humans ; MicroRNAs ; Arsenic ; Carcinogenesis
Chemical Substances	MicroRNAs ; Arsenic (N712M78A8G)
Language	English
Publishing date	2023-02-06
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural
ISSN	1557-8925
ISSN (online)	1557-8925
DOI	10.1016/bs.apha.2022.10.002
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Article ; Online: Clonal variability in chromosomal instability as a potential driver in the acquisition of tumorigenic phenotype in chronic arsenic-exposed and hsa-miR-186 overexpressing human keratinocytes.

Lykoudi, Angeliki / Ferragut Cardoso, Ana P / Wise, Sandra S / Banerjee, Mayukh / States, J Christopher

Toxicology and applied pharmacology

2023 Volume 479, Page(s) 116730

Abstract: Chronic arsenic exposure through drinking water is a global health issue, affecting >200 million people. Arsenic is a group I human carcinogen and causes chromosomal instability (CIN). Arsenic exposure is the second most common cause of skin cancer after ...

Abstract	Chronic arsenic exposure through drinking water is a global health issue, affecting >200 million people. Arsenic is a group I human carcinogen and causes chromosomal instability (CIN). Arsenic exposure is the second most common cause of skin cancer after UV radiation. hsa-miR-186 is overexpressed in arsenic-induced squamous cell carcinoma relative to premalignant hyperkeratosis. Among predicted targets of hsa-miR-186 are cell cycle regulators including regulators of mitotic progression. Disruption of mitotic progression can contribute to CIN. Thus, we hypothesized that hsa-miR-186 overexpression contributes to malignant transformation of arsenic exposed HaCaT cells by induction of CIN. Stable clones of HaCaT cells transfected with pEP-hsa-miR-186 expression vector or empty vector were maintained under puromycin selection and exposed to 0 or 100 nM NaAsO
MeSH term(s)	Humans ; Arsenic/toxicity ; Arsenic/metabolism ; Cell Line ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Carcinogenesis/genetics ; Keratinocytes/metabolism ; Clone Cells ; Phenotype ; Chromosomal Instability
Chemical Substances	MIRN186 microRNA, human ; Arsenic (N712M78A8G) ; MicroRNAs
Language	English
Publishing date	2023-10-20
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.2023.116730
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Article ; Online: miR-186 induces tetraploidy in arsenic exposed human keratinocytes.

Ferragut Cardoso, Ana P / Nail, Alexandra N / Banerjee, Mayukh / Wise, Sandra S / States, J Christopher

Ecotoxicology and environmental safety

2023 Volume 256, Page(s) 114823

Abstract: Chronic inorganic arsenic (iAs) exposure in drinking water is a global issue affecting >225 million people. Skin is a major target organ for iAs. miRNA dysregulation and chromosomal instability (CIN) are proposed mechanisms of iAs-induced carcinogenesis. ...

Abstract	Chronic inorganic arsenic (iAs) exposure in drinking water is a global issue affecting >225 million people. Skin is a major target organ for iAs. miRNA dysregulation and chromosomal instability (CIN) are proposed mechanisms of iAs-induced carcinogenesis. CIN is a cancer hallmark and tetraploid cells can better tolerate increase in chromosome number and aberration, contributing to the evolution of CIN. miR-186 is overexpressed in iAs-induced squamous cell carcinoma relative to iAs-induced hyperkeratosis. Bioinformatic analysis indicated that miR-186 targets mRNAs of important cell cycle regulators including mitotic checkpoint serine/threonine kinase B (BUB1) and cell division cycle 27 (CDC27). We hypothesized that miR-186 overexpression contributes to iAs-induced transformation of keratinocytes by targeting mitotic regulators leading to induction of CIN. Ker-CT cells, a near diploid human keratinocyte cell line, were transduced with miR-186 overexpressing or scrambled control lentivirus. Stable clones were isolated after puromycin selection. Clones transduced with lentivirus expressing either a scrambled control miRNA or miR-186 were maintained with 0 or 100 nM iAs for 4 weeks. Unexposed scrambled control clones were considered as passage matched controls. Chronic iAs exposure increased miR-186 expression in miR-186 clones. miR-186 overexpression significantly reduced CDC27 levels irrespective of iAs exposure. The percentage of tetraploid or aneuploid cells was increased in iAs exposed miR-186 clones. Aneuploidy can arise from a tetraploid intermediate. Suppression of CDC27 by miR-186 may lead to impairment of mitotic checkpoint complex formation and its ability to maintain cell cycle arrest leading to chromosome misalignment. As a result, cells overexpressing miR-186 and chronically exposed to iAs may have incorrect chromosome segregation and CIN. These data suggest that dysregulation of miRNA by iAs mediates tetraploidy, aneuploidy and chromosomal instability contributing to iAs-induced carcinogenesis.
MeSH term(s)	Humans ; Arsenic ; Tetraploidy ; MicroRNAs/genetics ; Aneuploidy ; Carcinogenesis ; Keratinocytes ; Chromosomal Instability
Chemical Substances	Arsenic (N712M78A8G) ; MicroRNAs ; MIRN186 microRNA, human
Language	English
Publishing date	2023-03-27
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	436536-7
ISSN	1090-2414 ; 0147-6513
ISSN (online)	1090-2414
ISSN	0147-6513
DOI	10.1016/j.ecoenv.2023.114823
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