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  1. Artikel ; Online: Iron overload in alcoholic liver disease: underlying mechanisms, detrimental effects, and potential therapeutic targets.

    Li, Long-Xia / Guo, Fang-Fang / Liu, Hong / Zeng, Tao

    Cellular and molecular life sciences : CMLS

    2022  Band 79, Heft 4, Seite(n) 201

    Abstract: Alcoholic liver disease (ALD) is a global public health challenge due to the high incidence and lack of effective therapeutics. Evidence from animal studies and ALD patients has demonstrated that iron overload is a hallmark of ALD. Ethanol exposure can ... ...

    Abstract Alcoholic liver disease (ALD) is a global public health challenge due to the high incidence and lack of effective therapeutics. Evidence from animal studies and ALD patients has demonstrated that iron overload is a hallmark of ALD. Ethanol exposure can promote iron absorption by downregulating the hepcidin expression, which is probably mediated by inducing oxidative stress and promoting erythropoietin (EPO) production. In addition, ethanol may enhance iron uptake in hepatocytes by upregulating the expression of transferrin receptor (TfR). Iron overload in the liver can aggravate ethanol-elicited liver damage by potentiating oxidative stress via Fenton reaction, promoting activation of Kupffer cells (KCs) and hepatic stellate cells (HSCs), and inducing a recently discovered programmed iron-dependent cell death, ferroptosis. This article reviews the current knowledge of iron metabolism, regulators of iron homeostasis, the mechanism of ethanol-induced iron overload, detrimental effects of iron overload in the liver, and potential therapeutic targets.
    Mesh-Begriff(e) Animals ; Hepatocytes/metabolism ; Humans ; Iron/metabolism ; Iron Overload/complications ; Iron Overload/therapy ; Liver Diseases, Alcoholic/metabolism
    Chemische Substanzen Iron (E1UOL152H7)
    Sprache Englisch
    Erscheinungsdatum 2022-03-24
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-022-04239-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 195: Hefte anzeigen Standort:
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  2. Artikel: Iron overload in alcoholic liver disease: underlying mechanisms, detrimental effects, and potential therapeutic targets

    Li, Long-Xia / Guo, Fang-Fang / Liu, Hong / Zeng, Tao

    Cellular and molecular life sciences. 2022 Apr., v. 79, no. 4

    2022  

    Abstract: Alcoholic liver disease (ALD) is a global public health challenge due to the high incidence and lack of effective therapeutics. Evidence from animal studies and ALD patients has demonstrated that iron overload is a hallmark of ALD. Ethanol exposure can ... ...

    Abstract Alcoholic liver disease (ALD) is a global public health challenge due to the high incidence and lack of effective therapeutics. Evidence from animal studies and ALD patients has demonstrated that iron overload is a hallmark of ALD. Ethanol exposure can promote iron absorption by downregulating the hepcidin expression, which is probably mediated by inducing oxidative stress and promoting erythropoietin (EPO) production. In addition, ethanol may enhance iron uptake in hepatocytes by upregulating the expression of transferrin receptor (TfR). Iron overload in the liver can aggravate ethanol-elicited liver damage by potentiating oxidative stress via Fenton reaction, promoting activation of Kupffer cells (KCs) and hepatic stellate cells (HSCs), and inducing a recently discovered programmed iron-dependent cell death, ferroptosis. This article reviews the current knowledge of iron metabolism, regulators of iron homeostasis, the mechanism of ethanol-induced iron overload, detrimental effects of iron overload in the liver, and potential therapeutic targets.
    Schlagwörter animals ; erythropoietin ; ethanol ; ferroptosis ; hepatocytes ; hepcidin ; homeostasis ; iron absorption ; iron overload ; liver ; liver diseases ; oxidative stress ; public health ; therapeutics ; transferrin receptors
    Sprache Englisch
    Erscheinungsverlauf 2022-04
    Umfang p. 201.
    Erscheinungsort Springer International Publishing
    Dokumenttyp Artikel
    Anmerkung Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-022-04239-9
    Datenquelle NAL Katalog (AGRICOLA)

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  3. Artikel ; Online: N,N-dimethylformamide-induced acute liver damage is driven by the activation of NLRP3 inflammasome in liver macrophages of mice.

    Liu, Hong / Li, Ming-Jun / Zhang, Xiu-Ning / Wang, Shuo / Li, Long-Xia / Guo, Fang-Fang / Zeng, Tao

    Ecotoxicology and environmental safety

    2022  Band 238, Seite(n) 113609

    Abstract: N,N-dimethylformamide (DMF) is a non-negligible volatile hazardous material in indoor and outdoor environments. Although the hepatotoxicity of DMF has been well recognized, the underlying mechanisms remain unclear and prophylactic medicine is still ... ...

    Abstract N,N-dimethylformamide (DMF) is a non-negligible volatile hazardous material in indoor and outdoor environments. Although the hepatotoxicity of DMF has been well recognized, the underlying mechanisms remain unclear and prophylactic medicine is still lacking. Herein, we established a DMF-induced acute liver injury mouse model and investigated the underlying mechanisms focusing on oxidative stress and the nucleotide-binding domain and leucine-rich repeat receptor (NLR) family pyrin domain (PYD)-containing 3 (NLRP3) inflammasome. DMF was found to induce oxidative stress, evidenced by the elevation of hepatic malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) adducts levels, and the decline of reduced glutathione (GSH) levels. However, neither N-acetyl cysteine (NAC) nor sulforaphane (SF) ameliorated the hepatoxicity induced by DMF in mice. Interestingly, DMF exposure led to focal necrosis of hepatocytes and NLRP3 inflammasome activation before the onset of obvious liver damage. In addition, DMF exposure induced infiltration and proinflammatory/M1 polarization of macrophages in mice livers. Furthermore, the inactivation of hepatic macrophages by GdCl
    Mesh-Begriff(e) Animals ; Chemical and Drug Induced Liver Injury/etiology ; Dimethylformamide ; Inflammasomes ; Liver ; Liver Diseases ; Macrophages ; Mice ; NLR Family, Pyrin Domain-Containing 3 Protein
    Chemische Substanzen Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Dimethylformamide (8696NH0Y2X)
    Sprache Englisch
    Erscheinungsdatum 2022-05-10
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ZDB-ID 436536-7
    ISSN 1090-2414 ; 0147-6513
    ISSN (online) 1090-2414
    ISSN 0147-6513
    DOI 10.1016/j.ecoenv.2022.113609
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Allyl methyl disulfide (AMDS) prevents N,N-dimethyl formamide-induced liver damage by suppressing oxidative stress and NLRP3 inflammasome activation.

    Li, Long-Xia / Wang, Lin / Wang, Shuo / Zhang, Xiu-Ning / Liu, Hong / Zhang, Yan-Jing / Wu, Chuan-Tao / Zhang, Cui-Li / Zeng, Tao

    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

    2023  Band 182, Seite(n) 114198

    Abstract: N,N-dimethylformamide (DMF), a widely consumed industrial solvent with persistent characteristics, can induce occupational liver damage and pose threats to the general population due to the enormous DMF-containing industrial efflux and emission from ... ...

    Abstract N,N-dimethylformamide (DMF), a widely consumed industrial solvent with persistent characteristics, can induce occupational liver damage and pose threats to the general population due to the enormous DMF-containing industrial efflux and emission from indoor facilities. This study was performed to explore the roles of allyl methyl disulfide (AMDS) in liver damage induced by DMF and the underlying mechanisms. AMDS was found to effectively suppress the elevation in the liver weight/body weight ratio and serum aminotransferase activities, and reduce the mortality of mice induced by DMF. In addition, AMDS abrogated DMF-elicited increases in malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) levels and decreases in glutathione (GSH) levels in mouse livers. The increase in macrophage number, mRNA expression of M1 macrophage biomarkers, and protein expression of key components in the NF-κB pathway and NLRP3 inflammasome induced by DMF exposure were all suppressed by AMDS in mouse livers. Furthermore, AMDS inhibited DMF-induced cell damage and NF-κB activation in cocultured AML12 hepatocytes and J774A.1 macrophages. However, AMDS per se did not significantly affect the protein level and activity of CYP2E1. Collectively, these results demonstrate that AMDS effectively ameliorates DMF-induced acute liver damage possibly by suppressing oxidative stress and inactivating the NF-κB pathway and NLRP3 inflammasome.
    Mesh-Begriff(e) Humans ; Mice ; Animals ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; NF-kappa B/metabolism ; Dimethylformamide/toxicity ; Dimethylformamide/metabolism ; Liver Diseases/metabolism ; Oxidative Stress ; Liver ; Glutathione/metabolism
    Chemische Substanzen Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NF-kappa B ; allyl methyl disulfide (OXW45UTR7B) ; Dimethylformamide (8696NH0Y2X) ; Glutathione (GAN16C9B8O)
    Sprache Englisch
    Erscheinungsdatum 2023-11-21
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 782617-5
    ISSN 1873-6351 ; 0278-6915
    ISSN (online) 1873-6351
    ISSN 0278-6915
    DOI 10.1016/j.fct.2023.114198
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 529: Hefte anzeigen Standort:
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  5. Artikel: Effect of erythropoietin on hepcidin, DMT1 with IRE, and hephaestin gene expression in duodenum of rats.

    Kong, Wei-Na / Chang, Yan-Zhong / Wang, Shu-Min / Zhai, Xing-Li / Shang, Jian-Xiu / Li, Long-Xia / Duan, Xiang-Lin

    Journal of gastroenterology

    2008  Band 43, Heft 2, Seite(n) 136–143

    Abstract: Background: Erythropoietin (Epo) is the central regulator of red blood cell production and can stimulate proliferation and differentiation of erythroid progenitor cells. Now, recombinant human erythropoietin (rHuEpo) is widely used in patients with ... ...

    Abstract Background: Erythropoietin (Epo) is the central regulator of red blood cell production and can stimulate proliferation and differentiation of erythroid progenitor cells. Now, recombinant human erythropoietin (rHuEpo) is widely used in patients with renal disease, chronic anemia, and iron deficiency of early childhood. It has been reported that the enhanced erythropoiesis associated with erythropoietin therapy increases intestinal iron absorption, but the molecular mechanisms underlying are unknown. Therefore, we have investigated the effect of rHuEpo on duodenal iron transport protein synthesis in rats.
    Methods: Male Sprague-Dawley rats weighing 250 g were randomly divided into two groups: (1) rHuEpo injection group (rHuEpo, 500 IU/day, s.c.), and (2) control group (injection of the same volume of saline). After 3 days injection, blood parameters, serum iron status, and non-heme iron concentrations in the liver and duodenum were examined at the fifth day. The mRNA levels and protein synthesis of duodenal divalent metal transporter 1 (DMT1), ferroportin 1 (FPN1), and hephaestin (Hp) were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analysis. Hepatic hepcidin mRNA expression was analyzed by RT-PCR.
    Results: rHuEpo injection significantly stimulated erythropoiesis and decreased serum iron status, non-heme iron concentrations in the liver and duodenum. DMT1 (+IRE) and Hp expression in duodenum were increased significantly. However, DMT1 (-IRE) and FPN1 expression had no apparent change. Hepatic hepcidin mRNA expression was decreased dramatically, reaching an almost undetectable level in rHuEpo-treated rats.
    Conclusions: rHuEpo administration improved the duodenal iron absorption by increasing the expression of DMT1 (+IRE) and Hp.
    Mesh-Begriff(e) Animals ; Antimicrobial Cationic Peptides/genetics ; Antimicrobial Cationic Peptides/metabolism ; Blotting, Western ; Cation Transport Proteins/genetics ; Cation Transport Proteins/metabolism ; Duodenum/drug effects ; Duodenum/metabolism ; Erythropoietin/pharmacology ; Gene Expression Regulation/drug effects ; Hematinics/pharmacology ; Hepcidins ; Immunohistochemistry ; Intestinal Absorption/drug effects ; Iron-Regulatory Proteins/genetics ; Iron-Regulatory Proteins/metabolism ; Male ; Membrane Proteins/metabolism ; Models, Animal ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins ; Reverse Transcriptase Polymerase Chain Reaction
    Chemische Substanzen Antimicrobial Cationic Peptides ; Cation Transport Proteins ; HAMP protein, human ; Hamp protein, rat ; Hematinics ; Hepcidins ; Heph, protein, rat ; Iron-Regulatory Proteins ; Membrane Proteins ; Recombinant Proteins ; solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2 ; Erythropoietin (11096-26-7)
    Sprache Englisch
    Erscheinungsdatum 2008-02-29
    Erscheinungsland Japan
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1186495-3
    ISSN 0944-1174
    ISSN 0944-1174
    DOI 10.1007/s00535-007-2138-5
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 620: Hefte anzeigen Standort:
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