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Article ; Online: Leveraging oxidative stress questions in vivo: Implications and limitations.

Arteel, Gavin E

2016 Volume 595, Page(s) 40–45

Abstract: ... understood that ROS/RNS are critical for normal cellular metabolism and have beneficial effects (e.g ...

Abstract	The elegance of Helmut Sies' original definition of oxidative stress belies the complexity of the reactions that are potentially involved. This is by no means a criticism of the author, but rather how the words have been used to oversimplify the concept by some. Reactive oxygen and nitrogen species (ROS and RNS, respectively) can be products of a myriad of events within the living body. Indeed, it is now understood that ROS/RNS are critical for normal cellular metabolism and have beneficial effects (e.g., cytotoxicity against invading bacteria). A general problem of studying prooxidants in vivo is that, due to their inherent reactivity, they generally cannot be measured directly. This indirect detection of 'footprints' leaves a very large black box that we are to this day only beginning to understand. This manuscript will summarize some considerations that are of utmost importance when translating oxidative stress into in vivo research. Helmut has been a key thought leader, researcher and mentor whose contributions to this field are immeasurable.
MeSH term(s)	Animals ; Humans ; Kinetics ; Oxidative Stress ; Reactive Nitrogen Species/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Nitrogen Species ; Reactive Oxygen Species
Language	English
Publishing date	2016-04-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2015.11.009
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Article: Leveraging oxidative stress questions inÂ vivo: Implications and limitations

Arteel, Gavin E

Archives of biochemistry and biophysics. 2016 Apr. 01, v. 595

2016

Abstract: ... understood that ROS/RNS are critical for normal cellular metabolism and have beneficial effects (e.g ...

Abstract	The elegance of Helmut Sies' original definition of oxidative stress belies the complexity of the reactions that are potentially involved. This is by no means a criticism of the author, but rather how the words have been used to oversimplify the concept by some. Reactive oxygen and nitrogen species (ROS and RNS, respectively) can be products of a myriad of events within the living body. Indeed, it is now understood that ROS/RNS are critical for normal cellular metabolism and have beneficial effects (e.g., cytotoxicity against invading bacteria). A general problem of studying prooxidants inÂ vivo is that, due to their inherent reactivity, they generally cannot be measured directly. This indirect detection of âfootprintsâ leaves a very large black box that we are to this day only beginning to understand. This manuscript will summarize some considerations that are of utmost importance when translating oxidative stress into inÂ vivo research. Helmut has been a key thought leader, researcher and mentor whose contributions to this field are immeasurable.
Keywords	bacteria ; cytotoxicity ; leaves ; metabolism ; nitrogen ; oxidative stress ; oxygen
Language	English
Dates of publication	2016-0401
Size	p. 40-45.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2015.11.009
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Article ; Online: Transitional Remodeling of the Hepatic Extracellular Matrix in Alcohol-Induced Liver Injury.

Poole, Lauren G / Arteel, Gavin E

BioMed research international

2016 Volume 2016, Page(s) 3162670

Abstract: Alcohol consumption is a common custom worldwide, and the toxic effects of alcohol on several target organs are well understood. The liver is the primary site of alcohol metabolism and is therefore the major target of alcohol toxicity. Alcoholic liver ... ...

Abstract	Alcohol consumption is a common custom worldwide, and the toxic effects of alcohol on several target organs are well understood. The liver is the primary site of alcohol metabolism and is therefore the major target of alcohol toxicity. Alcoholic liver disease is a spectrum of disease states, ranging from simple steatosis (fat accumulation), to inflammation, and eventually to fibrosis and cirrhosis if untreated. The fibrotic stage of ALD is primarily characterized by robust accumulation of extracellular matrix (ECM) proteins (collagens) which ultimately impairs the function of the organ. The role of the ECM in early stages of ALD is poorly understood, but recent research has demonstrated that a number of changes in the hepatic ECM in prefibrotic ALD not only are present, but may also contribute to disease progression. The purpose of this review is to summarize the established and proposed changes to the hepatic extracellular matrix (ECM) that may contribute to earlier stages of ALD development and to discuss potential mechanisms by which these changes may mediate the progression of the disease.
MeSH term(s)	Animals ; Disease Progression ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Extracellular Matrix Proteins/metabolism ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Diseases, Alcoholic/metabolism ; Liver Diseases, Alcoholic/pathology ; Models, Biological
Chemical Substances	Extracellular Matrix Proteins
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2016/3162670
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Article ; Online: Organ-Organ Crosstalk and Alcoholic Liver Disease.

Poole, Lauren G / Dolin, Christine E / Arteel, Gavin E

Biomolecules

2017 Volume 7, Issue 3

Abstract: ... alcoholic liver disease (ALD) (i.e., alcoholic hepatitis (AH) and cirrhosis), additional research is required to develop ...

Abstract	Alcohol consumption is a common custom worldwide, and the toxic effects of alcohol on several target organs are well-understood. Given the poor prognosis of treating clinically-relevant alcoholic liver disease (ALD) (i.e., alcoholic hepatitis (AH) and cirrhosis), additional research is required to develop more effective therapies. While the stages of ALD have been well-characterized, targeted therapies to prevent or reverse this process in humans are still needed. Better understanding of risk factors and mechanisms underlying disease progression can lead to the development of rational therapies to prevent or reverse ALD in the clinic. A potential area of targeted therapy for ALD may be organ-organ communication in the early stages of the disease. In contrast to AH and end-stage liver diseases, the involvement of multiple organs in the development of ALD is less understood. The impact of these changes on pathology to the liver and other organs may not only influence disease progression during the development of the disease, but also outcomes of end stages diseases. The purpose of this review is to summarize the established and proposed communication between the liver and other organ systems that may contribute to the development and progression of liver disease, as well as to other organs. Potential mechanisms of this organ-organ communication are also discussed.
MeSH term(s)	Biomarkers, Tumor/metabolism ; Cell Communication/drug effects ; Cytokines/metabolism ; Disease Progression ; Extracellular Vesicles/metabolism ; Humans ; Liver Diseases, Alcoholic/drug therapy ; Liver Diseases, Alcoholic/metabolism ; Liver Diseases, Alcoholic/pathology ; Risk Factors
Chemical Substances	Biomarkers, Tumor ; Cytokines
Language	English
Publishing date	2017-08-16
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom7030062
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Article ; Online: Animal models of alcoholic liver disease.

Arteel, Gavin E

Digestive diseases (Basel, Switzerland)

2011 Volume 28, Issue 6, Page(s) 729–736

Abstract: ... the advent of genetically modified strains of rodents (e.g. 'knockout' mice) has increased the specificity ...

Abstract	The risk of alcohol-induced liver disease (ALD) increases dose- and time-dependently with consumption of alcohol. The progression of the disease is well characterized; however, although the progression of alcohol-induced liver injury is well characterized, there is no universally-accepted therapy available to halt or reverse this process in humans. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of this disease, rational targeted therapy can be developed to treat or prevent it in the clinics. Several models for experimental ALD exist, including non-human primates, micropigs and rodents. However, most researchers employ rodent models of ALD. Furthermore, the advent of genetically modified strains of rodents (e.g. 'knockout' mice) has increased the specificity of the hypotheses that can be directly tested. Based on these models systems, several plausible hypotheses to explain the mechanism(s) by which alcohol leads to liver damage have been proposed, including consequences of alcohol metabolism, oxidative/nitrosative stress, altered inflammatory responses, and increased sensitivity to cytotoxic stimuli. These studies have also identified candidate genes for polymorphism studies to explain potential increased genetic risk in some individuals. However, despite significant advances in our understanding of the mechanisms by which ALD develops based on studies with these models, this work has yet to translate to a viable therapy for ALD in the clinics. This talk will also discuss potential reasons for these limitations to date and suggest future prospects to improve the translational utility of modeling ALD.
MeSH term(s)	Acute Disease ; Animals ; Chronic Disease ; Disease Models, Animal ; Ethanol/administration & dosage ; Humans ; Liver Diseases, Alcoholic/pathology
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2011-04-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	632798-9
ISSN	1421-9875 ; 0257-2753
ISSN (online)	1421-9875
ISSN	0257-2753
DOI	10.1159/000324280
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Article: The biochemistry of selenium and the glutathione system.

Arteel, G E / Sies, H

Environmental toxicology and pharmacology

2011 Volume 10, Issue 4, Page(s) 153–158

Abstract: ... other selenoproteins (e.g. selenoprotein P and thioredoxin reductase) also have been shown to possess antioxidant ... properties. Synthetic organoselenium compounds (e.g. ebselen) have also shown promise as pharmacologic ...

Abstract	In the context of defense against pro-oxidants, selenium and the glutathione (GSH) system play key functions. Major roles of GSH include direct interception of pro-oxidants, as well as a reduction of other antioxidants from their oxidized forms. Furthermore, GSH has ancillary functions, such as metabolism, cell signaling, and protein interactions, that can also mediate defense against oxidants. Protection by selenium in the mammalian cell is mediated by selenol-aminoacids, either as selenocysteine or selenomethionine. The active site of the potent glutathione peroxidases (GPx) contains selenocysteine residues. Furthermore, other selenoproteins (e.g. selenoprotein P and thioredoxin reductase) also have been shown to possess antioxidant properties. Synthetic organoselenium compounds (e.g. ebselen) have also shown promise as pharmacologic antioxidants in in vivo models of tissue damage due to oxidative stress. The specific function of selenoproteins and organoselenium compounds in defense against peroxynitrite, by reduction of this potent oxidizing and nitrating species to nitrite, is also discussed.
Language	English
Publishing date	2011-07-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1318302-3
ISSN	1382-6689
ISSN	1382-6689
DOI	10.1016/s1382-6689(01)00078-3
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Article: Animal Models of Alcoholic Liver Disease

Arteel, Gavin E.

Digestive Diseases

2011 Volume 28, Issue 6, Page(s) 729–736

Abstract: ... the advent of genetically modified strains of rodents (e.g. ‘knockout’ mice) has increased the specificity ...

Institution	Department of Pharmacology and Toxicology, The University of Louisville Alcohol Research Center, University of Louisville Health Sciences Center, Louisville, Ky., USA
Abstract	The risk of alcohol-induced liver disease (ALD) increases dose- and time-dependently with consumption of alcohol. The progression of the disease is well characterized; however, although the progression of alcohol-induced liver injury is well characterized, there is no universally-accepted therapy available to halt or reverse this process in humans. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of this disease, rational targeted therapy can be developed to treat or prevent it in the clinics. Several models for experimental ALD exist, including non-human primates, micropigs and rodents. However, most researchers employ rodent models of ALD. Furthermore, the advent of genetically modified strains of rodents (e.g. ‘knockout’ mice) has increased the specificity of the hypotheses that can be directly tested. Based on these models systems, several plausible hypotheses to explain the mechanism(s) by which alcohol leads to liver damage have been proposed, including consequences of alcohol metabolism, oxidative/nitrosative stress, altered inflammatory responses, and increased sensitivity to cytotoxic stimuli. These studies have also identified candidate genes for polymorphism studies to explain potential increased genetic risk in some individuals. However, despite significant advances in our understanding of the mechanisms by which ALD develops based on studies with these models, this work has yet to translate to a viable therapy for ALD in the clinics. This talk will also discuss potential reasons for these limitations to date and suggest future prospects to improve the translational utility of modeling ALD.
Keywords	Alcoholic liver disease ; Animal models ; Steatosis ; Inflammation ; Fibrosis
Language	English
Publishing date	2011-04-27
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Pathomechanisms of Alcohol-Induced Damage
ZDB-ID	632798-9
ISBN	978-3-8055-9732-6 ; 978-3-8055-9733-3 ; 3-8055-9732-0 ; 3-8055-9733-9
ISSN	1421-9875 ; 0257-2753
ISSN (online)	1421-9875
ISSN	0257-2753
DOI	10.1159/000324280
Database	Karger publisher's database

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Article ; 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 Volume 468, Page(s) 116514

Abstract: ... Conclusions: These data indicate that VC sensitizes the liver to other stressors (e.g., WD), resulting ... However, lower exposure levels (i.e., sub-regulatory exposure limits) that do not directly damage the liver ...

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 term(s)	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
Chemical Substances	Vinyl Chloride (WD06X94M2D)
Language	English
Publishing date	2023-04-14
Publishing country	United States
Document type	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
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Article ; Online: Adipose tissue-liver crosstalk during pathologic changes caused by vinyl chloride metabolites in mice.

Kaelin, Brenna R / McKenzie, Collin M / Hempel, Karl W / Lang, Anna L / Arteel, Gavin E / Beier, Juliane I

Toxicology and applied pharmacology

2020 Volume 399, Page(s) 115068

Abstract: ... correlated with increased expression of lipid-associated proteins (e.g., PLINs). CE also enhanced HFD-induced ...

Abstract	Volatile organic compounds (VOCs), such as vinyl chloride (VC), can be directly toxic at high concentrations. However, we have shown that 'nontoxic' exposures to VC and its metabolite chloroethanol (CE) enhances experimental non-alcoholic fatty liver disease (NAFLD), suggesting an unpredicted interaction. Importantly, VOC exposure has been identified as a potential risk factor for the development of obesity and its sequelae in humans. As there is a known axis between adipose and hepatic tissue in NAFLD, the impact of CE on white adipose tissue (WAT) inflammation and lipolysis was investigated. Mice were administered CE (or vehicle) once, after 10 weeks of being fed high-fat or low-fat diet (LFD). CE significantly enhanced hepatic steatosis and inflammation caused by HFD. HFD significantly increased the size of epididymal fat pads, which was enhanced by CE. The relative size of adipocyte lipid droplets increased by HFD + CE, which was also correlated with increased expression of lipid-associated proteins (e.g., PLINs). CE also enhanced HFD-induced indices of WAT inflammation, and ER stress. Hepatic-derived circulating FGF21, a major modulator of WAT lipolysis, which is hypothesized to thereby regulate hepatic steatosis, was significantly increased by CE in animals fed HFD. Taken together these data support the hypothesis that environmental toxicant exposure can exacerbate the severity of NAFLD/NASH, involving the liver-adipose axis in this process. Specifically, CE enhances local inflammation and alters lipid metabolism and WAT-mediated hepatic steatosis due to changes in WAT lipolysis.
MeSH term(s)	Adipocytes/drug effects ; Adipocytes/metabolism ; Adipose Tissue, White/drug effects ; Adipose Tissue, White/metabolism ; Animals ; Diet, High-Fat/adverse effects ; Inflammation/chemically induced ; Inflammation/metabolism ; Lipid Metabolism/drug effects ; Lipids ; Liver/drug effects ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease/metabolism ; Obesity/chemically induced ; Obesity/metabolism ; Vinyl Chloride/toxicity
Chemical Substances	Lipids ; Vinyl Chloride (WD06X94M2D)
Language	English
Publishing date	2020-05-20
Publishing country	United States
Document type	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.2020.115068
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Article ; Online: WNT7B Regulates Cholangiocyte Proliferation and Function During Murine Cholestasis.

Kosar, Karis / Cornuet, Pamela / Singh, Sucha / Lee, Elizabeth / Liu, Silvia / Gayden, Jenesis / Sato, Toshifumi / Freyberg, Zachary / Arteel, Gavin / Nejak-Bowen, Kari

Hepatology communications

2021 Volume 5, Issue 12, Page(s) 2019–2034

Abstract: We previously identified an up-regulation of specific Wnt proteins in the cholangiocyte compartment during cholestatic liver injury and found that mice lacking Wnt secretion from hepatocytes and cholangiocytes showed fewer proliferating cholangiocytes ... ...

Abstract	We previously identified an up-regulation of specific Wnt proteins in the cholangiocyte compartment during cholestatic liver injury and found that mice lacking Wnt secretion from hepatocytes and cholangiocytes showed fewer proliferating cholangiocytes and high mortality in response to a 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet, a murine model of primary sclerosing cholangitis. In vitro studies demonstrated that Wnt7b, one of the Wnts up-regulated during cholestasis, induces proliferation of cholangiocytes in an autocrine manner and increases secretion of proinflammatory cytokines. We hypothesized that loss of Wnt7b may exacerbate some of the complications of cholangiopathies by decreasing the ability of bile ducts to induce repair. Wnt7b-flox mice were bred with Krt19-cre mice to deplete Wnt7b expression in only cholangiocytes (CC) or with albumin-Cre mice to delete Wnt7b expression in both hepatocytes and cholangiocytes (HC + CC). These mice were placed on a DDC diet for 1 month then killed for evaluation. Contrary to our expectations, we found that mice lacking Wnt7b from CC and HC + CC compartments had improved biliary injury, decreased cellular senescence, and lesser bile acid accumulation after DDC exposure compared to controls, along with decreased expression of inflammatory cytokines. Although Wnt7b knockout (KO) resulted in fewer proliferating cholangiocytes, CC and HC + CC KO mice on a DDC diet also had more hepatocytes expressing cholangiocyte markers compared to wild-type mice on a DDC diet, indicating that Wnt7b suppression promotes hepatocyte reprogramming. Conclusion: Wnt7b induces a proproliferative proinflammatory program in cholangiocytes, and its loss is compensated for by conversion of hepatocytes to a biliary phenotype during cholestatic injury.
MeSH term(s)	Animals ; Bile Acids and Salts/metabolism ; Bile Ducts/cytology ; Cell Proliferation/genetics ; Cellular Senescence/genetics ; Cholestasis/genetics ; Disease Models, Animal ; Hepatocytes/metabolism ; Mice ; Mice, Knockout ; Proto-Oncogene Proteins/deficiency ; Wnt Proteins/deficiency
Chemical Substances	Bile Acids and Salts ; Proto-Oncogene Proteins ; Wnt Proteins ; Wnt7b protein, mouse
Language	English
Publishing date	2021-08-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2471-254X
ISSN (online)	2471-254X
DOI	10.1002/hep4.1784
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