Manganese Superoxide Dismutase Dimorphism and Iron Overload, Hepatocellular Carcinoma, and Death in Hepatitis C Virus–Infected Patients

2007 ◽  
Vol 5 (5) ◽  
pp. 630-635 ◽  
Author(s):  
Pierre Nahon ◽  
Angela Sutton ◽  
Dominique Pessayre ◽  
Pierre Rufat ◽  
Marianne Ziol ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Superoxide Dismutase ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Iron Overload ◽  
Manganese Superoxide Dismutase ◽  
Manganese Superoxide

Induced oxidative stress and activated expression of manganese superoxide dismutase during hepatitis C virus replication: role of JNK, p38 MAPK and AP-1

2004 ◽  
Vol 381 (3) ◽  
pp. 951-951
Author(s):  
I. QADRI ◽  
M. IWAHASHI ◽  
J. M. CAPASSO ◽  
M. W. HOPKEN ◽  
S. FLORES ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
P38 Mapk ◽  
Virus Replication ◽  
Manganese Superoxide Dismutase ◽  
Manganese Superoxide

scholarly journals Induced oxidative stress and activated expression of manganese superoxide dismutase during hepatitis C virus replication: role of JNK, p38 MAPK and AP-1

2004 ◽  
Vol 378 (3) ◽  
pp. 919-928 ◽  
Author(s):  
Ishtiaq QADRI ◽  
Mieko IWAHASHI ◽  
Juan M. CAPASSO ◽  
Matthew W. HOPKEN ◽  
Sonia FLORES ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
P38 Mapk ◽  
Cellular Response ◽  
Manganese Superoxide Dismutase ◽  
Fold Increase ◽  
Subgenomic Replicon ◽  
Manganese Superoxide

Activation of cellular kinases and transcription factors mediates the early phase of the cellular response to chemically or biologically induced stress. In the present study we investigated the oxidant/antioxidant balance in Huh-7 cells expressing the HCV (hepatitis C virus) subgenomic replicon, and observed a 5-fold increase in oxidative stress during HCV replication. We used MnSOD (manganese-superoxide dismutase) as an indicator of the cellular antioxidant response, and found that its activity, protein levels and promoter activity were significantly increased, whereas Cu/ZnSOD was not affected. The oxidative stress-induced protein kinases p38 MAPK (mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase) were activated in the HCV repliconcontaining cells and in Huh-7 cells transduced with Ad-NS5A [a recombinant adenovirus encoding NS5A (non-structural protein 5A)], coupled with a 4–5-fold increase in AP-1 (activator protein-1) DNA binding. Ava.1 cells, which encode a replication-defective HCV replicon, showed no significant changes in MnSOD, p38 MAPK or JNK activity. The AP-1 inhibitors dithiothreitol and N-acetylcysteine, as well as a dominant negative AP-1 mutant, significantly reduced AP-1 activation, demonstrating that this activation is oxidative stress-related. Exogenous NS5A had no effect on AP-1 activation in vitro, suggesting that NS5A acts at the upstream targets of AP-1 involving p38 MAPK and JNK signalling cascades. AP-1-dependent gene expression was increased in HCV subgenomic replicon-expressing Huh-7 cells. MnSOD activation was blocked by inhibitors of JNK (JNKI1) and p38 MAPK (SB203580), but not by an ERK (extracellular-signal-regulated kinase) inhibitor (U0126), in HCV-replicating and Ad-NS5A-transduced cells. Our results demonstrate that cellular responses to oxidative stress in HCV subgenomic replicon-expressing and Ad-NS5A-transduced cells are regulated by two distinct signalling pathways involving p38 MAPK and JNK via AP-1 that is linked to increased oxidative stress and therefore to an increased antioxidant MnSOD response.

Mechanisms of Liver Injury. III. Oxidative stress in the pathogenesis of hepatitis C virus

2006 ◽  
Vol 290 (5) ◽  
pp. G847-G851 ◽  
Author(s):  
Jinah Choi ◽  
J.-H. James Ou
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Liver Injury ◽  
Iron Overload ◽  
Antioxidant Defense ◽  
Hcv Infection ◽  
Nitrogen Species ◽  
Systemic Oxidative Stress

Hepatitis C virus (HCV) is a major cause of viral hepatitis that can progress to hepatic fibrosis, steatosis, hepatocellular carcinoma, and liver failure. HCV infection is characterized by a systemic oxidative stress that is most likely caused by a combination of chronic inflammation, iron overload, liver damage, and proteins encoded by HCV. The increased generation of reactive oxygen and nitrogen species, together with the decreased antioxidant defense, promotes the development and progression of hepatic and extrahepatic complications of HCV infection. This review discusses the possible mechanisms of HCV-induced oxidative stress and its role in HCV pathogenesis.

Immunohistochemical expression of manganese superoxide dismutase in hepatocellular carcinoma, using a specific monoclonal antibody

1994 ◽  
Vol 29 (4) ◽  
pp. 443-449 ◽  
Author(s):  
Yoshi Aida ◽  
Shiro Maeyama ◽  
Toshifumi Takakuwa ◽  
Toshiyuki Uchikoshi ◽  
Yasuo Endo ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Monoclonal Antibody ◽  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Specific Monoclonal Antibody ◽  
Immunohistochemical Expression ◽  
Manganese Superoxide

Different Roles of Sp Family Members in HIV-1 Tat-Mediated Manganese Superoxide Dismutase Suppression in Hepatocellular Carcinoma Cells

2005 ◽  
Vol 24 (5) ◽  
pp. 299-310 ◽  
Author(s):  
Sureerut Porntadavity ◽  
Avindra Nath ◽  
Virapong Prachayasittikul ◽  
Adela Cota-Gomez ◽  
Sonia C. Flores ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Family Members ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Manganese Superoxide ◽  
Hiv 1

scholarly journals 17β-Estradiol Promotes Apoptosis of HepG2 Cells Caused by Oxidative Stress by Increasing Foxo3a Phosphorylation

2021 ◽  
Vol 12 ◽  
Author(s):  
Yusheng Guo ◽  
Xiangsheng Cai ◽  
Hanwei Lu ◽  
Qiqi Li ◽  
Ying Zheng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Superoxide Dismutase ◽  
Hepg2 Cells ◽  
Manganese Superoxide Dismutase ◽  
Manganese Superoxide ◽  
B Virus ◽  
17Β Estradiol ◽  
New Treatment

Liver cancer is associated with high mortality, particularly in patients infected with the hepatitis B virus. Treatment methods remain very limited. Here, we explored the effects of 17β-estradiol (E2) on apoptosis of various liver cell lines (LO2, HepG2, and HepG2.2.15 cells). Within a certain concentration range, 17β-estradiol induced oxidative stress and apoptosis of HepG2 cells, downregulated ERα-36 expression, and increased Akt and Foxo3a phosphorylation. p-Foxo3a became localized around the nucleus but did not enter the organelle. The levels of mRNAs encoding manganese superoxide dismutase (MnSOD) and catalase, to the promoters of which Foxo3a binds to trigger gene expression, were significantly reduced in HepG2 cells. 17β-estradiol had no obvious effects on LO2 or HepG2.2.15 cells. We speculate that 17β-estradiol may induce oxidative stress in HepG2 cells by increasing Foxo3a phosphorylation, thus promoting apoptosis. This may serve as a new treatment for hepatocellular carcinoma.

Hepatic Iron Overload Induces Hepatocellular Carcinoma in Transgenic Mice Expressing the Hepatitis C Virus Polyprotein

2006 ◽  
Vol 130 (7) ◽  
pp. 2087-2098 ◽  
Author(s):  
Takakazu Furutani ◽  
Keisuke Hino ◽  
Michiari Okuda ◽  
Toshikazu Gondo ◽  
Sohji Nishina ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Transgenic Mice ◽  
Iron Overload ◽  
Hepatic Iron ◽  
Hepatic Iron Overload ◽  
Virus Polyprotein

Manganese superoxide dismutase activity and incidence of hepatocellular carcinoma in patients with Child?Pugh class A liver cirrhosis: a 7-year follow-up study

2007 ◽  
Vol 27 (6) ◽  
pp. 791-797 ◽  
Author(s):  
Caterina Clemente ◽  
Silvana Elba ◽  
Gianpiero Buongiorno ◽  
Vito Guerra ◽  
Benedetta D'Attoma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Superoxide Dismutase ◽  
Liver Cirrhosis ◽  
Manganese Superoxide Dismutase ◽  
Superoxide Dismutase Activity ◽  
Follow Up Study ◽  
Class A ◽  
Manganese Superoxide ◽  
Pugh Class
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