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  1. AU="Schnegelberger, Regina D"
  2. AU=Doshi Paresh
  3. AU="Cecilia Hognon"
  4. AU="Mason, Jeremy K."
  5. AU=Hasumi Hisashi
  6. AU="Swati Sethi"
  7. AU="Martin G. Myers, Jr."
  8. AU="Marcus-Sekura, Carol"
  9. AU="Petagine, Lucy"
  10. AU="Jessa R. Alexander"
  11. AU=Rauner Martina
  12. AU="Richlen, Mindy L"
  13. AU="Merghani, Nada M"
  14. AU=Splitt M P
  15. AU="Zlatanović, Gordana"

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  1. Artikel: Using a competitive counterflow assay to identify novel cationic substrates of OATP1B1 and OATP1B3.

    Schnegelberger, Regina D / Steiert, Brianna / Sandoval, Philip J / Hagenbuch, Bruno

    Frontiers in physiology

    2022  Band 13, Seite(n) 969363

    Abstract: OATP1B1 and OATP1B3 are two drug transporters that mediate the uptake of multiple endo- and xenobiotics, including many drugs, into human hepatocytes. Numerous inhibitors have been identified, and for some of them, it is not clear whether they are also ... ...

    Abstract OATP1B1 and OATP1B3 are two drug transporters that mediate the uptake of multiple endo- and xenobiotics, including many drugs, into human hepatocytes. Numerous inhibitors have been identified, and for some of them, it is not clear whether they are also substrates. Historically radiolabeled substrates or LC-MS/MS methods were needed to test for transported substrates, both of which can be limiting in time and money. However, the competitive counterflow (CCF) assay originally described for OCT2 and, more recently, for OCT1, OATP2B1, and OATP1A2 does not require radiolabeled substrates or LC-MS/MS methods and, as a result, is a more cost-effective approach to identifying substrates of multidrug transporters. We used a CCF assay based on the stimulated efflux of the common model substrate estradiol-17β-glucuronide (E17βG) and tested 30 compounds for OATP1B1- and OATP1B3-mediated transport. Chinese Hamster Ovary (CHO) cells stably expressing OATP1B1 or OATP1B3 were preloaded with 10 nM [
    Sprache Englisch
    Erscheinungsdatum 2022-09-08
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2022.969363
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Environmental toxicant-induced maladaptive mitochondrial changes: A potential unifying mechanism in fatty liver disease?

    Schnegelberger, Regina D / Lang, Anna L / Arteel, Gavin E / Beier, Juliane I

    Acta pharmaceutica Sinica. B

    2021  Band 11, Heft 12, Seite(n) 3756–3767

    Abstract: Occupational and environmental exposures to industrial chemicals are well known to cause hepatotoxicity and liver injury. However, despite extensive evidence showing that exposure can lead to disease, current research approaches and regulatory policies ... ...

    Abstract Occupational and environmental exposures to industrial chemicals are well known to cause hepatotoxicity and liver injury. However, despite extensive evidence showing that exposure can lead to disease, current research approaches and regulatory policies fail to address the possibility that subtle changes caused by low level exposure to chemicals may also enhance preexisting conditions. In recent years, the conceptual understanding of the contribution of environmental chemicals to liver disease has progressed significantly. Mitochondria are often target of toxicity of environmental toxicants resulting in multisystem disorders involving different cells, tissues, and organs. Here, we review persistent maladaptive changes to mitochondria in response to environmental toxicant exposure as a mechanism of hepatotoxicity. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of toxicant-induced liver disease, rational targeted therapy can be developed to better predict risk, as well as to treat or prevent this disease.
    Sprache Englisch
    Erscheinungsdatum 2021-09-08
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Review
    ISSN 2211-3835
    ISSN 2211-3835
    DOI 10.1016/j.apsb.2021.09.002
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Vinyl Chloride and High-Fat Diet as a Model of Environment and Obesity Interaction.

    Lang, Anna L / Goldsmith, William T / Schnegelberger, Regina D / Arteel, Gavin E / Beier, Juliane I

    Journal of visualized experiments : JoVE

    2020  , Heft 155

    Abstract: Vinyl chloride (VC), an abundant environmental contaminant, causes steatohepatitis at high levels, but is considered safe at lower levels. Although several studies have investigated the role of VC as a direct hepatotoxicant, the concept that VC modifies ... ...

    Abstract Vinyl chloride (VC), an abundant environmental contaminant, causes steatohepatitis at high levels, but is considered safe at lower levels. Although several studies have investigated the role of VC as a direct hepatotoxicant, the concept that VC modifies sensitivity of the liver to other factors, such as nonalcoholic fatty liver disease (NAFLD) caused by high-fat diet (HFD) is novel. This protocol describes an exposure paradigm to evaluate the effects of chronic, low-level exposure to VC. Mice are acclimated to low-fat or high-fat diet one week prior to the beginning of the inhalation exposure and remain on these diets throughout the experiment. Mice are exposed to VC (sub-OSHA level: <1 ppm) or room air in inhalation chambers for 6 hours/day, 5 days/week, for up to 12 weeks. Animals are monitored weekly for body weight gain and food consumption. This model of VC exposure causes no overt liver injury with VC inhalation alone. However, the combination of VC and HFD significantly enhances liver disease. A technical advantage of this co-exposure model is the whole-body exposure, without restraint. Moreover, the conditions more closely resemble a very common human situation of a combined exposure to VC with underlying nonalcoholic fatty liver disease and therefore support the novel hypothesis that VC is an environmental risk factor for the development of liver damage as a complication of obesity (i.e., NAFLD). This work challenges the paradigm that the current exposure limits of VC (occupational and environmental) are safe. The use of this model can shed new light and concern on the risks of VC exposure. This model of toxicant-induced liver injury can be used for other volatile organic compounds and to study other interactions that may impact the liver and other organ systems.
    Mesh-Begriff(e) Administration, Inhalation ; Animals ; Diet, High-Fat/adverse effects ; Environmental Exposure ; Humans ; Liver/drug effects ; Liver/injuries ; Liver/pathology ; Liver Diseases/etiology ; Mice, Inbred C57BL ; Models, Biological ; Obesity/etiology ; Vinyl Chloride/toxicity
    Chemische Substanzen Vinyl Chloride (WD06X94M2D)
    Sprache Englisch
    Erscheinungsdatum 2020-01-12
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Video-Audio Media
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/60351
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Vinyl chloride and high-fat diet as a model of environment and obesity interaction

    Lang, Anna L / Goldsmith, William T / Schnegelberger, Regina D / Arteel, Gavin E / Beier, Juliane I

    Journal of visualized experiments. 2020 Jan. 12, , no. 155

    2020  

    Abstract: Vinyl chloride (VC), an abundant environmental contaminant, causes steatohepatitis at high levels, but is considered safe at lower levels. Although several studies have investigated the role of VC as a direct hepatotoxicant, the concept that VC modifies ... ...

    Abstract Vinyl chloride (VC), an abundant environmental contaminant, causes steatohepatitis at high levels, but is considered safe at lower levels. Although several studies have investigated the role of VC as a direct hepatotoxicant, the concept that VC modifies sensitivity of the liver to other factors, such as nonalcoholic fatty liver disease (NAFLD) caused by high-fat diet (HFD) is novel. This protocol describes an exposure paradigm to evaluate the effects of chronic, low-level exposure to VC. Mice are acclimated to low-fat or high-fat diet one week prior to the beginning of the inhalation exposure and remain on these diets throughout the experiment. Mice are exposed to VC (sub-OSHA level: <1 ppm) or room air in inhalation chambers for 6 hours/day, 5 days/week, for up to 12 weeks. Animals are monitored weekly for body weight gain and food consumption. This model of VC exposure causes no overt liver injury with VC inhalation alone. However, the combination of VC and HFD significantly enhances liver disease. A technical advantage of this co-exposure model is the whole-body exposure, without restraint. Moreover, the conditions more closely resemble a very common human situation of a combined exposure to VC with underlying nonalcoholic fatty liver disease and therefore support the novel hypothesis that VC is an environmental risk factor for the development of liver damage as a complication of obesity (i.e., NAFLD). This work challenges the paradigm that the current exposure limits of VC (occupational and environmental) are safe. The use of this model can shed new light and concern on the risks of VC exposure. This model of toxicant-induced liver injury can be used for other volatile organic compounds and to study other interactions that may impact the liver and other organ systems.
    Schlagwörter air ; body weight changes ; fatty liver ; feed intake ; high fat diet ; humans ; inhalation exposure ; liver ; mice ; models ; obesity ; organochlorine compounds ; risk factors ; vinyl chloride ; volatile organic compounds
    Sprache Englisch
    Erscheinungsverlauf 2020-0112
    Umfang p. e60351.
    Erscheinungsort Journal of Visualized Experiments
    Dokumenttyp Artikel
    ZDB-ID 2259946-0
    ISSN 1940-087X
    ISSN 1940-087X
    DOI 10.3791/60351
    Datenquelle NAL Katalog (AGRICOLA)

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  5. Artikel ; Online: Western diet unmasks transient low-level vinyl chloride-induced tumorigenesis; potential role of the (epi-)transcriptome.

    Liu, Silvia / He, Liqing / Bannister, Olivia B / Li, Jiang / Schnegelberger, Regina D / Vanderpuye, Charis-Marie / Althouse, Andrew D / Schopfer, Francisco J / Wahlang, Banrida / Cave, Matthew C / Monga, Satdarshan P / Zhang, Xiang / Arteel, Gavin E / Beier, Juliane I

    Toxicology and applied pharmacology

    2023  Band 468, Seite(n) 116514

    Abstract: Background & aims: Vinyl chloride (VC) monomer is a volatile organic compound commonly used in industry. At high exposure levels, VC causes liver cancer and toxicant-associated steatohepatitis. However, lower exposure levels (i.e., sub-regulatory ... ...

    Abstract Background & aims: Vinyl chloride (VC) monomer is a volatile organic compound commonly used in industry. At high exposure levels, VC causes liver cancer and toxicant-associated steatohepatitis. However, lower exposure levels (i.e., sub-regulatory exposure limits) that do not directly damage the liver, enhance injury caused by Western diet (WD). It is still unknown if the long-term impact of transient low-concentration VC enhances the risk of liver cancer development. This is especially a concern given that fatty liver disease is in and of itself a risk factor for the development of liver cancer.
    Methods: C57Bl/6 J mice were fed WD or control diet (CD) for 1 year. During the first 12 weeks of feeding only, mice were also exposed to VC via inhalation at sub-regulatory limit concentrations (<1 ppm) or air for 6 h/day, 5 days/week.
    Results: Feeding WD for 1 year caused significant hepatic injury, which was exacerbated by VC. Additionally, VC increased the number of tumors which ranged from moderately to poorly differentiated hepatocellular carcinoma (HCC). Transcriptomic analysis demonstrated VC-induced changes in metabolic but also ribosomal processes. Epitranscriptomic analysis showed a VC-induced shift of the modification pattern that has been associated with metabolic disease, mitochondrial dysfunction, and cancer.
    Conclusions: These data indicate that VC sensitizes the liver to other stressors (e.g., WD), resulting in enhanced tumorigenesis. These data raise concerns about potential interactions between VC exposure and WD. It also emphasizes that current safety restrictions may be insufficient to account for other factors that can influence hepatotoxicity.
    Mesh-Begriff(e) Mice ; Animals ; Vinyl Chloride/toxicity ; Vinyl Chloride/metabolism ; Transcriptome ; Carcinoma, Hepatocellular/pathology ; Diet, Western ; Liver Neoplasms/chemically induced ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Carcinogenesis/metabolism ; Cell Transformation, Neoplastic/metabolism
    Chemische Substanzen Vinyl Chloride (WD06X94M2D)
    Sprache Englisch
    Erscheinungsdatum 2023-04-14
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2023.116514
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Rapamycin attenuates liver injury caused by vinyl chloride metabolite chloroethanol and lipopolysaccharide in mice.

    Lang, Anna L / Krueger, Austin M / Schnegelberger, Regina D / Kaelin, Brenna R / Rakutt, Maxwell J / Chen, Liya / Arteel, Gavin E / Beier, Juliane I

    Toxicology and applied pharmacology

    2019  Band 382, Seite(n) 114745

    Abstract: Vinyl chloride (VC) is a prevalent environmental toxicant that is rapidly metabolized within the liver. Its metabolites have been shown to directly cause hepatic injury at high exposure levels. We have previously reported that VC metabolite, ... ...

    Abstract Vinyl chloride (VC) is a prevalent environmental toxicant that is rapidly metabolized within the liver. Its metabolites have been shown to directly cause hepatic injury at high exposure levels. We have previously reported that VC metabolite, chloroethanol (CE), potentiates liver injury caused by lipopolysaccharide (LPS). Importantly, that study showed that CE alone, while not causing damage per se, was sufficient to alter hepatic metabolism and increase mTOR phosphorylation in mice, suggesting a possible role for the mTOR pathway. Here, we explored the effect of an mTOR inhibitor, rapamycin, in this model. C57BL/6 J mice were administered CE, followed by rapamycin 1 h and LPS 24 h later. As observed previously, the combination of CE and LPS significantly enhanced liver injury, inflammation, oxidative stress, and metabolic dysregulation. Rapamycin attenuated not only inflammation, but also restored the metabolic phenotype and protected against CE + LPS-induced oxidative stress. Importantly, rapamycin protected against mitochondrial damage and subsequent production of reactive oxygen species (ROS). The protective effect on mitochondrial function by rapamycin was mediated, by restoring the integrity of the electron transport chain at least in part, by blunting the deactivation of mitochondrial c-src, which is involved mitochondrial ROS production by electron transport chain leakage. Taken together, these results further demonstrate a significant role of mTOR-mediated pathways in VC-metabolite induced liver injury and provide further insight into VC-associated hepatic damage. As mTOR mediated pathways are very complex and rapamycin is a more global inhibitor, more specific mTOR (i.e. mTORC1) inhibitors should be considered in future studies.
    Mesh-Begriff(e) Animals ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/prevention & control ; Chlorides/toxicity ; Ethanol/toxicity ; Lipopolysaccharides/toxicity ; Male ; Mice ; Mice, Inbred C57BL ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Sirolimus/pharmacology ; Sirolimus/therapeutic use ; Vinyl Chloride/metabolism ; Vinyl Chloride/toxicity
    Chemische Substanzen Chlorides ; Lipopolysaccharides ; Ethanol (3K9958V90M) ; Sirolimus (W36ZG6FT64) ; Vinyl Chloride (WD06X94M2D)
    Sprache Englisch
    Erscheinungsdatum 2019-09-06
    Erscheinungsland United States
    Dokumenttyp 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.2019.114745
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Mechanisms of Environmental Contributions to Fatty Liver Disease.

    Wahlang, Banrida / Jin, Jian / Beier, Juliane I / Hardesty, Josiah E / Daly, Erica F / Schnegelberger, Regina D / Falkner, K Cameron / Prough, Russell A / Kirpich, Irina A / Cave, Matthew C

    Current environmental health reports

    2019  Band 6, Heft 3, Seite(n) 80–94

    Abstract: Purpose: Fatty liver disease (FLD) affects over 25% of the global population and may lead to liver-related mortality due to cirrhosis and liver cancer. FLD caused by occupational and environmental chemical exposures is termed "toxicant-associated ... ...

    Abstract Purpose: Fatty liver disease (FLD) affects over 25% of the global population and may lead to liver-related mortality due to cirrhosis and liver cancer. FLD caused by occupational and environmental chemical exposures is termed "toxicant-associated steatohepatitis" (TASH). The current review addresses the scientific progress made in the mechanistic understanding of TASH since its initial description in 2010.
    Recent findings: Recently discovered modes of actions for volatile organic compounds and persistent organic pollutants include the following: (i) the endocrine-, metabolism-, and signaling-disrupting chemical hypotheses; (ii) chemical-nutrient interactions and the "two-hit" hypothesis. These key hypotheses were then reviewed in the context of the steatosis adverse outcome pathway (AOP) proposed by the US Environmental Protection Agency. The conceptual understanding of the contribution of environmental exposures to FLD has progressed significantly. However, because this is a new research area, more studies including mechanistic human data are required to address current knowledge gaps.
    Mesh-Begriff(e) Carcinogens/toxicity ; Endocrine Disruptors/adverse effects ; Environmental Exposure/adverse effects ; Environmental Pollutants/toxicity ; Humans ; Non-alcoholic Fatty Liver Disease/chemically induced ; Non-alcoholic Fatty Liver Disease/epidemiology ; Pesticides/toxicity ; Risk Factors
    Chemische Substanzen Carcinogens ; Endocrine Disruptors ; Environmental Pollutants ; Pesticides
    Sprache Englisch
    Erscheinungsdatum 2019-05-25
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Review
    ISSN 2196-5412
    ISSN (online) 2196-5412
    DOI 10.1007/s40572-019-00232-w
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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