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Book ; Thesis: Analysis of the activation mechanisms of immune relevant cells following exposure to 50 Hz magnetic fields

Lupke, Madeleine

2005

Title variant	Fifty Hertz
Author's details	vorgelegt von Madeleine Lupke
Language	English
Size	Getr. Zählung, Ill., graph. Darst.
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Math.-Naturwiss. Fak., Diss.--Rostock, 2006
Note	Enth. 5 Beitr. aus versch. Ztschr.
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Augmenter of Liver Regeneration Reduces Ischemia Reperfusion Injury by Less Chemokine Expression, Gr-1 Infiltration and Oxidative Stress.

Weiss, Thomas S / Lupke, Madeleine / Dayoub, Rania / Geissler, Edward K / Schlitt, Hans J / Melter, Michael / Eggenhofer, Elke

Cells

2019 Volume 8, Issue 11

Abstract: Hepatic ischemia reperfusion injury (IRI) is a major complication in liver resection and transplantation. Here, we analyzed the impact of recombinant human augmenter of liver regeneration (rALR), an anti-oxidative and anti-apoptotic protein, on the ... ...

Abstract	Hepatic ischemia reperfusion injury (IRI) is a major complication in liver resection and transplantation. Here, we analyzed the impact of recombinant human augmenter of liver regeneration (rALR), an anti-oxidative and anti-apoptotic protein, on the deleterious process induced by ischemia reperfusion (IR). Application of rALR reduced tissue damage (necrosis), levels of lipid peroxidation (oxidative stress) and expression of anti-oxidative genes in a mouse IRI model. Damage associated molecule pattern (DAMP) and inflammatory cytokines such as HMGB1 and TNFα, were not affected by rALR. Furthermore, we evaluated infiltration of inflammatory cells into liver tissue after IRI and found no change in CD3 or γδTCR positive cells, or expression of IL17/IFNγ by γδTCR cells. The quantity of Gr-1 positive cells (neutrophils), and therefore, myeloperoxidase activity, was lower in rALR-treated mice. Moreover, we found under hypoxic conditions attenuated ROS levels after ALR treatment in RAW264.7 cells and in primary mouse hepatocytes. Application of rALR also led to reduced expression of chemo-attractants like CXCL1, CXCL2 and CCl2 in hepatocytes. In addition, ALR expression was increased in IR mouse livers after 3 h and in biopsies from human liver transplants with minimal signs of tissue damage. Therefore, ALR attenuates IRI through reduced neutrophil tissue infiltration mediated by lower expression of key hepatic chemokines and reduction of ROS generation.
MeSH term(s)	Animals ; Antigens, Ly/metabolism ; Apoptosis/genetics ; Biopsy ; Chemokines/genetics ; Chemokines/metabolism ; Disease Models, Animal ; Flow Cytometry ; Hepatocytes/metabolism ; Immunohistochemistry ; Liver/metabolism ; Liver/pathology ; Liver Regeneration/genetics ; Male ; Mice ; Models, Biological ; Neutrophils/immunology ; Neutrophils/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Reperfusion Injury/etiology ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Antigens, Ly ; Chemokines ; Reactive Oxygen Species
Language	English
Publishing date	2019-11-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8111421
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Attenuated lipotoxicity and apoptosis is linked to exogenous and endogenous augmenter of liver regeneration by different pathways.

Weiss, Thomas S / Lupke, Madeleine / Ibrahim, Sara / Buechler, Christa / Lorenz, Julia / Ruemmele, Petra / Hofmann, Ute / Melter, Michael / Dayoub, Rania

PloS one

2017 Volume 12, Issue 9, Page(s) e0184282

Abstract: Nonalcoholic fatty liver disease (NAFLD) covers a spectrum from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. Free fatty acids (FFA) induce steatosis and lipo-toxicity and correlate with severity of NAFLD. In this study we aimed ... ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) covers a spectrum from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. Free fatty acids (FFA) induce steatosis and lipo-toxicity and correlate with severity of NAFLD. In this study we aimed to investigate the role of exogenous and endogenous ALR (augmenter of liver regeneration) for FFA induced ER (endoplasmatic reticulum) -stress and lipoapoptosis. Primary human hepatocytes or hepatoma cells either treated with recombinant human ALR (rhALR, 15kDa) or expressing short form ALR (sfALR, 15kDa) were incubated with palmitic acid (PA) and analyzed for lipo-toxicity, -apoptosis, activation of ER-stress response pathways, triacylglycerides (TAG), mRNA and protein expression of lipid metabolizing genes. Both, exogenous rhALR and cytosolic sfALR reduced PA induced caspase 3 activity and Bax protein expression and therefore lipotoxicity. Endogenous sfALR but not rhALR treatment lowered TAG levels, diminished activation of ER-stress mediators C-Jun N-terminal kinase (JNK), X-box binding protein-1 (XBP1) and proapoptotic transcription factor C/EBP-homologous protein (CHOP), and reduced death receptor 5 protein expression. Cellular ALR exerts its lipid lowering and anti-apoptotic actions by enhancing FABP1, which binds toxic FFA, increasing mitochondrial β-oxidation by elevating the mitochondrial FFA transporter CPT1α, and decreasing ELOVL6, which delivers toxic FFA metabolites. We found reduced hepatic mRNA levels of ALR in a high fat diet mouse model, and of ALR and FOXA2, a transcription factor inducing ALR expression, in human steatotic as well as NASH liver samples, which may explain increased lipid deposition and reduced β-oxidation in NASH patients. Present study shows that exogenous and endogenous ALR reduce PA induced lipoapoptosis. Furthermore, cytosolic sfALR changes mRNA and protein expression of genes regulating lipid metabolism, reduces ER-stress finally impeding progression of NASH.
MeSH term(s)	Animals ; Apoptosis ; Caspase 3/metabolism ; Cytosol/metabolism ; Dithiothreitol/chemistry ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress ; Fatty Acids, Nonesterified/metabolism ; Gene Expression Regulation ; Hep G2 Cells ; Hepatocyte Nuclear Factor 3-beta/metabolism ; Hepatocytes/cytology ; Humans ; Lipid Metabolism ; Lipoproteins/metabolism ; Liver/metabolism ; Liver Regeneration ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; RNA, Messenger/metabolism ; Rats ; Recombinant Proteins/metabolism ; Thapsigargin/chemistry ; Triglycerides/metabolism ; Tunicamycin/chemistry ; bcl-2-Associated X Protein/metabolism
Chemical Substances	BAX protein, human ; FOXA2 protein, human ; Fatty Acids, Nonesterified ; Foxa2 protein, mouse ; Lipoproteins ; RNA, Messenger ; Recombinant Proteins ; Triglycerides ; bcl-2-Associated X Protein ; Tunicamycin (11089-65-9) ; Hepatocyte Nuclear Factor 3-beta (135845-92-0) ; Thapsigargin (67526-95-8) ; CASP3 protein, human (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Dithiothreitol (T8ID5YZU6Y)
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0184282
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Augmenter of Liver Regeneration Reduces Ischemia Reperfusion Injury by Less Chemokine Expression, Gr-1 Infiltration and Oxidative Stress

Weiss, Thomas S. / Lupke, Madeleine / Dayoub, Rania / Geissler, Edward K. / Schlitt, Hans J. / Melter, Michael / Eggenhofer, Elke

Fraunhofer ITEM

2019

Abstract	Hepatic ischemia reperfusion injury (IRI) is a major complication in liver resection and transplantation. Here, we analyzed the impact of recombinant human augmenter of liver regeneration (rALR), an anti-oxidative and anti-apoptotic protein, on the deleterious process induced by ischemia reperfusion (IR). Application of rALR reduced tissue damage (necrosis), levels of lipid peroxidation (oxidative stress) and expression of anti-oxidative genes in a mouse IRI model. Damage associated molecule pattern (DAMP) and inflammatory cytokines such as HMGB1 and TNFα, were not affected by rALR. Furthermore, we evaluated infiltration of inflammatory cells into liver tissue after IRI and found no change in CD3 or γδTCR positive cells, or expression of IL17/IFNγ by γδTCR cells. The quantity of Gr-1 positive cells (neutrophils), and therefore, myeloperoxidase activity, was lower in rALR-treated mice. Moreover, we found under hypoxic conditions attenuated ROS levels after ALR treatment in RAW264.7 cells and in primary mouse hepatocytes. Application of rALR also led to reduced expression of chemo-attractants like CXCL1, CXCL2 and CCl2 in hepatocytes. In addition, ALR expression was increased in IR mouse livers after 3 h and in biopsies from human liver transplants with minimal signs of tissue damage. Therefore, ALR attenuates IRI through reduced neutrophil tissue infiltration mediated by lower expression of key hepatic chemokines and reduction of ROS generation.
Keywords	ischemia reperfusion ; liver regeneration ; Chemokines ; neutrophils ; oxidative stress
Subject code	610
Language	English
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Augmenter of Liver Regeneration Reduces Ischemia Reperfusion Injury by Less Chemokine Expression, Gr-1 Infiltration and Oxidative Stress

Weiss, Thomas S. / Lupke, Madeleine / Dayoub, Rania / Geissler, Edward K. / Schlitt, Hans J. / Melter, Michael / Eggenhofer, Elke

2019

Abstract: Art. 1421, 15 S. ... Hepatic ischemia reperfusion injury (IRI) is a major complication in liver resection and transplantation. Here, we analyzed the impact of recombinant human augmenter of liver regeneration (rALR), an anti-oxidative and anti-apoptotic ... ...

Abstract	Art. 1421, 15 S. Hepatic ischemia reperfusion injury (IRI) is a major complication in liver resection and transplantation. Here, we analyzed the impact of recombinant human augmenter of liver regeneration (rALR), an anti-oxidative and anti-apoptotic protein, on the deleterious process induced by ischemia reperfusion (IR). Application of rALR reduced tissue damage (necrosis), levels of lipid peroxidation (oxidative stress) and expression of anti-oxidative genes in a mouse IRI model. Damage associated molecule pattern (DAMP) and inflammatory cytokines such as HMGB1 and TNFa, were not affected by rALR. Furthermore, we evaluated infiltration of inflammatory cells into liver tissue after IRI and found no change in CD3 or gdTCR positive cells, or expression of IL17/IFNg by gdTCR cells. The quantity of Gr-1 positive cells (neutrophils), and therefore, myeloperoxidase activity, was lower in rALR-treated mice. Moreover, we found under hypoxic conditions attenuated ROS levels after ALR treatment in RAW264.7 cells and in primary mouse hepatocytes. Application of rALR also led to reduced expression of chemo-attractants like CXCL1, CXCL2 and CCl2 in hepatocytes. In addition, ALR expression was increased in IR mouse livers after 3 h and in biopsies from human liver transplants with minimal signs of tissue damage. Therefore, ALR attenuates IRI through reduced neutrophil tissue infiltration mediated by lower expression of key hepatic chemokines and reduction of ROS generation. 8 Nr.11
Keywords	ischemia reperfusion ; liver regeneration ; Chemokines ; neutrophils ; oxidative stress ; 610 ; 620
Subject code	610
Language	English
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Manganese superoxide dismutase is reduced in the liver of male but not female humans and rodents with non-alcoholic fatty liver disease

Krautbauer, Sabrina / Eisinger, Kristina / Lupke, Madeleine / Wanninger, Josef / Ruemmele, Petra / Hader, Yvonne / Weiss, Thomas S / Buechler, Christa

Experimental and molecular pathology. 2013 Dec., v. 95, no. 3

2013

Abstract: Non-alcoholic fatty liver disease (NAFLD) is among the most common liver diseases. Oxidative stress is one of the pathogenic mechanisms contributing to the progression of simple fatty liver to non-alcoholic steatohepatitis (NASH). Manganese superoxide ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) is among the most common liver diseases. Oxidative stress is one of the pathogenic mechanisms contributing to the progression of simple fatty liver to non-alcoholic steatohepatitis (NASH). Manganese superoxide dismutase (MnSOD) is a mitochondrial antioxidative enzyme and here its expression in rodent and human NAFLD has been analyzed. MnSOD is found reduced in the liver of male mice fed a high fat diet and male ob/ob mice. Female mice fed an atherogenic diet to induce NASH have MnSOD protein levels comparable to controls. In a cohort of 30 controls, 41 patients with fatty liver and 39 NASH patients, MnSOD mRNA is significantly lower in the steatotic and NASH liver. When analyzed in both genders separately reduction of MnSOD expression is only found in males. Here, MnSOD mRNA negatively correlates with steatosis grade but not with extent of fibrosis or inflammation. MnSOD is, however, not reduced in primary human hepatocytes (PHH) treated with palmitate or oleate to increase cellular triglycerides. Lipopolysaccharide, TNF, IL-6, TGFβ and leptin which are all raised in NAFLD do not affect MnSOD in PHH. Adiponectin which attenuates oxidative stress partly by increasing MnSOD in macrophages does not induce MnSOD in PHH. In summary, current data show that hepatic MnSOD is reduced in male but not female humans and rodents with NAFLD.
Keywords	adiponectin ; fatty liver ; females ; fibrosis ; hepatocytes ; high fat diet ; humans ; inflammation ; interleukin-6 ; leptin ; lipopolysaccharides ; liver ; macrophages ; males ; messenger RNA ; mice ; oleic acid ; oxidative stress ; patients ; superoxide dismutase ; transforming growth factor beta ; triacylglycerols
Language	English
Dates of publication	2013-12
Size	p. 330-335.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	207655-x
ISSN	1096-0945 ; 0014-4800
ISSN (online)	1096-0945
ISSN	0014-4800
DOI	10.1016/j.yexmp.2013.10.003
Database	NAL-Catalogue (AGRICOLA)

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Article: Cell activating capacity of 50 Hz magnetic fields to release reactive oxygen intermediates in human umbilical cord blood-derived monocytes and in Mono Mac 6 cells.

Lupke, Madeleine / Rollwitz, Jana / Simkó, Myrtill

Free radical research

2004 Volume 38, Issue 9, Page(s) 985–993

Abstract: The aim of this study was to investigate the mechanism of cell activation induced by extremely low frequency magnetic fields (ELF-MF) (50 Hz) in human cells. We examined the production of free radicals in human umbilical cord blood-derived monocytes and ... ...

Abstract	The aim of this study was to investigate the mechanism of cell activation induced by extremely low frequency magnetic fields (ELF-MF) (50 Hz) in human cells. We examined the production of free radicals in human umbilical cord blood-derived monocytes and in human Mono Mac 6 cells. The release of superoxide radical anions was analyzed using nitroblue tetrazolium chloride and the total of reactive oxygen species (ROS) was detected using dihydrorhodamine 123. Our results show a significant increase of superoxide radical anion production up-to 1.4 fold as well as an increase in ROS release up-to 1.2 fold upon exposure of monocytes to 1 mT ELF-MF (45 min). Mono Mac 6 cells exhibit higher superoxide radical anion and ROS production up-to 1.4 and 1.5 fold, respectively. These results indicate that Mono Mac 6 cells are more sensitive to ELF-MF than monocytes. Using diphenyleneiodonium chloride (DPI) a specific inhibitor for the NADPH oxidase, the MF-effect was not inhibited in Mono Mac 6 cells. Therefore, we suggest that ELF-MF exposure induces the activation of NADH oxidase in these cells. However, the MF-effect was inhibited by DPI in monocytes, indicating the activation of the NADPH oxidase after exposure to ELF-MF.
MeSH term(s)	Cell Line ; Cells, Cultured ; Electromagnetic Fields ; Enzyme Inhibitors/pharmacology ; Fetal Blood ; Flow Cytometry ; Humans ; Lipopolysaccharides ; Monocytes/metabolism ; Monocytes/radiation effects ; Multienzyme Complexes/metabolism ; NADH, NADPH Oxidoreductases/metabolism ; NADPH Oxidases/antagonists & inhibitors ; NADPH Oxidases/metabolism ; Onium Compounds/pharmacology ; Reactive Oxygen Species/metabolism ; Superoxides/metabolism ; Tetradecanoylphorbol Acetate
Chemical Substances	Enzyme Inhibitors ; Lipopolysaccharides ; Multienzyme Complexes ; Onium Compounds ; Reactive Oxygen Species ; Superoxides (11062-77-4) ; diphenyleneiodonium (6HJ411TU98) ; NADH oxidase (EC 1.6.-) ; NADH, NADPH Oxidoreductases (EC 1.6.-) ; NADPH Oxidases (EC 1.6.3.-) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2004-09
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1194130-3
ISSN	1029-2470 ; 1071-5762
ISSN (online)	1029-2470
ISSN	1071-5762
DOI	10.1080/10715760400000968
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Article: Fifty-hertz magnetic fields induce free radical formation in mouse bone marrow-derived promonocytes and macrophages.

Rollwitz, Jana / Lupke, Madeleine / Simkó, Myrtill

Biochimica et biophysica acta

2004 Volume 1674, Issue 3, Page(s) 231–238

Abstract: Our findings show a significant increase of free radical production after exposure to 50 Hz electromagnetic fields at a flux density of 1 mT to mouse bone marrow-derived (MBM) promonocytes and macrophages, indicating the cell-activating capacity of ... ...

Abstract	Our findings show a significant increase of free radical production after exposure to 50 Hz electromagnetic fields at a flux density of 1 mT to mouse bone marrow-derived (MBM) promonocytes and macrophages, indicating the cell-activating capacity of extremely low frequency magnetic fields (ELF-MF). We demonstrate that after exposure to ELF-MF mainly superoxide anion radicals were produced, both in MBM macrophages (33%) and also in their precursor cells (24%). To elucidate whether NADPH- or NADH-oxidase functions are target proteins for MF interaction, the flavoprotein inhibitor diphenyleneiodonium chloride (DPI) was used. MF-induced free radical production was not inhibited by DPI, whereas tetradecanoylphorbolacetate (TPA)-induced free radical production was diminished by about 70%. TPA is known to induce a direct activation of NADPH-oxidase through the PKC pathway. Since DPI lacks an inhibitory effect in MF-exposed MBM cells, we suggest that 50 Hz MF stimulates the NADH-oxidase pathway to produce superoxide anion radicals, but not the NADPH pathway. Furthermore, we showed an oscillation (1-10 days) in superoxide anion radical release in mouse macrophages, indicating a cyclic pattern of NADH-oxidase activity.
MeSH term(s)	Animals ; Bone Marrow Cells/cytology ; Bone Marrow Cells/radiation effects ; Electromagnetic Fields ; Free Radicals/metabolism ; Macrophages/cytology ; Macrophages/physiology ; Macrophages/radiation effects ; Mice ; Monocytes/cytology ; Monocytes/physiology ; Monocytes/radiation effects ; Multienzyme Complexes/metabolism ; Multienzyme Complexes/radiation effects ; NADH, NADPH Oxidoreductases/metabolism ; NADH, NADPH Oxidoreductases/radiation effects ; NADPH Oxidases/metabolism ; NADPH Oxidases/radiation effects ; Tetradecanoylphorbol Acetate/pharmacology
Chemical Substances	Free Radicals ; Multienzyme Complexes ; NADH oxidase (EC 1.6.-) ; NADH, NADPH Oxidoreductases (EC 1.6.-) ; NADPH Oxidases (EC 1.6.3.-) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2004-11-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagen.2004.06.024
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Article ; Online: Nrf2 activates augmenter of liver regeneration (ALR) via antioxidant response element and links oxidative stress to liver regeneration.

Dayoub, Rania / Vogel, Arndt / Schuett, Jutta / Lupke, Madeleine / Spieker, Susannah M / Kettern, Nadja / Hildt, Eberhard / Melter, Michael / Weiss, Thomas S

Molecular medicine (Cambridge, Mass.)

2013 Volume 19, Page(s) 237–244

Abstract: Liver regeneration can be impaired by permanent oxidative stress and activation of nuclear factor erythroid 2-related factor 2 (Nrf2), known to regulate the cellular antioxidant response, and has been shown to improve the process of liver regeneration. A ...

Abstract	Liver regeneration can be impaired by permanent oxidative stress and activation of nuclear factor erythroid 2-related factor 2 (Nrf2), known to regulate the cellular antioxidant response, and has been shown to improve the process of liver regeneration. A variety of factors regulate hepatic tissue regeneration, among them augmenter of liver regeneration (ALR), attained great attention as being survival factors for the liver with proproliferative and antiapoptotic properties. Here we determined the Nrf2/antioxidant response element (ARE) regulated expression of ALR and show ALR as a target gene of Nrf2 in vitro and in vivo. The ALR promoter comprises an ARE binding site and, therefore, ALR expression can be induced by ARE-activator tertiary butylhydroquinone (tBHQ) in hepatoma cells and primary human hepatocytes (PHH). Promoter activity and expression of ALR were enhanced after cotransfection of Nrf2 compared with control and dominant negative mutant of Nrf2. Performing partial hepatectomy in livers from Nrf2+/+ mice compared with Nrf2-/- knock-out (KO) mice, we found increased expression of ALR in addition to known antioxidant ARE-regulated genes. Furthermore, we observed increased ALR expression in hepatitis B virus (HBV) compared with hepatitis C virus (HCV) positive hepatoma cells and PHH. Recently, it was demonstrated that HBV infection activates Nrf2 and, now, we add results showing increased ALR expression in liver samples from patients infected with HBV. ALR is regulated by Nrf2, acts as a liver regeneration and antioxidative protein and, therefore, links oxidative stress to hepatic regeneration to ensure survival of damaged cells.
MeSH term(s)	Animals ; Antioxidant Response Elements ; Cell Line, Tumor ; Cells, Cultured ; Cytochrome Reductases/genetics ; Hepatitis B/metabolism ; Hepatitis C/metabolism ; Hepatocytes/metabolism ; Humans ; Liver/metabolism ; Liver Regeneration/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NF-E2-Related Factor 2/genetics ; Oxidative Stress/genetics ; Oxidoreductases Acting on Sulfur Group Donors
Chemical Substances	NF-E2-Related Factor 2 ; Cytochrome Reductases (EC 1.6.2.-) ; GFER protein, human (EC 1.8.-) ; Oxidoreductases Acting on Sulfur Group Donors (EC 1.8.-)
Language	English
Publishing date	2013-08-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.2119/molmed.2013.00027
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Article ; Online: Manganese superoxide dismutase is reduced in the liver of male but not female humans and rodents with non-alcoholic fatty liver disease.

Krautbauer, Sabrina / Eisinger, Kristina / Lupke, Madeleine / Wanninger, Josef / Ruemmele, Petra / Hader, Yvonne / Weiss, Thomas S / Buechler, Christa

Experimental and molecular pathology

2013 Volume 95, Issue 3, Page(s) 330–335

Abstract	Non-alcoholic fatty liver disease (NAFLD) is among the most common liver diseases. Oxidative stress is one of the pathogenic mechanisms contributing to the progression of simple fatty liver to non-alcoholic steatohepatitis (NASH). Manganese superoxide dismutase (MnSOD) is a mitochondrial antioxidative enzyme and here its expression in rodent and human NAFLD has been analyzed. MnSOD is found reduced in the liver of male mice fed a high fat diet and male ob/ob mice. Female mice fed an atherogenic diet to induce NASH have MnSOD protein levels comparable to controls. In a cohort of 30 controls, 41 patients with fatty liver and 39 NASH patients, MnSOD mRNA is significantly lower in the steatotic and NASH liver. When analyzed in both genders separately reduction of MnSOD expression is only found in males. Here, MnSOD mRNA negatively correlates with steatosis grade but not with extent of fibrosis or inflammation. MnSOD is, however, not reduced in primary human hepatocytes (PHH) treated with palmitate or oleate to increase cellular triglycerides. Lipopolysaccharide, TNF, IL-6, TGFβ and leptin which are all raised in NAFLD do not affect MnSOD in PHH. Adiponectin which attenuates oxidative stress partly by increasing MnSOD in macrophages does not induce MnSOD in PHH. In summary, current data show that hepatic MnSOD is reduced in male but not female humans and rodents with NAFLD.
MeSH term(s)	Adult ; Aged ; Animals ; Apoptosis ; Blotting, Western ; Case-Control Studies ; Cell Proliferation ; Cells, Cultured ; Cohort Studies ; Fatty Liver/enzymology ; Fatty Liver/pathology ; Female ; Hepatocytes/cytology ; Hepatocytes/metabolism ; Humans ; Leptin/physiology ; Liver/cytology ; Liver/enzymology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Middle Aged ; Non-alcoholic Fatty Liver Disease ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Superoxide Dismutase/metabolism ; Young Adult
Chemical Substances	Leptin ; RNA, Messenger ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2013-12
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207655-x
ISSN	1096-0945 ; 0014-4800
ISSN (online)	1096-0945
ISSN	0014-4800
DOI	10.1016/j.yexmp.2013.10.003
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

Order via subito