Diminished CCl 4 ‐induced hepatocellular carcinoma, oxidative stress, and apoptosis by co‐administration of curcumin or selenium in mice

2021 ◽  
Author(s):  
Asmaa Elkhamesy ◽  
Manar Refaat ◽  
Mona S. O. Gouida ◽  
Salma S. Alrdahe ◽  
Magdy M. Youssef
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma

CDCA2 protects against oxidative stress by promoting BRCA1–NRF2 signaling in hepatocellular carcinoma

Oncogene ◽  
2021 ◽  
Author(s):  
Shouping Wang ◽  
Kun Cao ◽  
Yuting Liao ◽  
Wei Zhang ◽  
Jihua Zheng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma

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.

Fumonisin B1-induced oxidative stress triggers Nrf2-mediated antioxidant response in human hepatocellular carcinoma (HepG2) cells

2018 ◽  
Vol 35 (1) ◽  
pp. 99-109 ◽  
Author(s):  
Thilona Arumugam ◽  
Yashodani Pillay ◽  
Terisha Ghazi ◽  
Savania Nagiah ◽  
Naeem Sheik Abdul ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Fumonisin B1 ◽  
Antioxidant Response ◽  
Human Hepatocellular Carcinoma

scholarly journals The Prognostic Role of Glutathione and Its Related Antioxidant Enzymes in the Recurrence of Hepatocellular Carcinoma

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4071
Author(s):  
Yung-Fang Hsiao ◽  
Shao-Bin Cheng ◽  
Chia-Yu Lai ◽  
Hsiao-Tien Liu ◽  
Shih-Chien Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Antioxidant Enzymes ◽  
Prognostic Significance ◽  
Tumor Resection ◽  
Trolox Equivalent Antioxidant Capacity ◽  
Antioxidant Capacities ◽  
The Impact ◽  
Hcc Recurrence

The imbalance of high oxidative stress and low antioxidant capacities is thought to be a significant cause of the development and progression of hepatocellular carcinoma (HCC). However, the impact of oxidative stress, glutathione (GSH), and its related antioxidant enzymes on the recurrence of HCC has not been investigated. The purpose of this study was to compare the changes to oxidative stress and GSH-related antioxidant capacities before and after tumor resection in patients with HCC recurrence and non-recurrence. We also evaluated the prognostic significance of GSH and its related enzymes in HCC recurrence. This was a cross-sectional and follow-up study. Ninety-two HCC patients who were going to receive tumor resection were recruited. We followed patients’ recurrence and survival status until the end of the study, and then assigned patients into the recurrent or the non-recurrent group. The tumor recurrence rate was 52.2% during the median follow-up period of 3.0 years. Patients had significantly lower plasma malondialdehyde level, but significantly or slightly higher levels of GSH, glutathione disulfide, trolox equivalent antioxidant capacity, glutathione peroxidase (GPx), and glutathione reductase (GR) activities after tumor resection compared to the respective levels before tumor resection in both recurrent and non-recurrent groups. GSH level in HCC tissue was significantly higher than that in adjacent normal tissue in both recurrent and non-recurrent patients. Decreased plasma GPx (HR = 0.995, p = 0.01) and GR (HR = 0.98, p = 0.04) activities before tumor resection, and the increased change of GPx (post—pre-resection) (HR = 1.004, p = 0.03) activity were significantly associated with the recurrence of HCC. These findings suggest there might be a possible application of GPx or GR as therapeutic targets for reducing HCC recurrence.

scholarly journals Gankyrin has an antioxidative role through the feedback regulation of Nrf2 in hepatocellular carcinoma

2016 ◽  
Vol 213 (5) ◽  
pp. 859-875 ◽  
Author(s):  
Chun Yang ◽  
Ye-xiong Tan ◽  
Guang-zhen Yang ◽  
Jian Zhang ◽  
Yu-fei Pan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Redox Homeostasis ◽  
Feedback Regulation ◽  
Cellular Redox ◽  
Intracellular Ros ◽  
Oxidative Stress Status ◽  
Kelch Domain ◽  
Cellular Stressors ◽  
Hcc Cells

Oxidative stress status has a key role in hepatocellular carcinoma (HCC) development and progression. Normally, reactive oxygen species (ROS) levels are tightly controlled by an inducible antioxidant program that responds to cellular stressors. How HCC cells respond to excessive oxidative stress remains elusive. Here, we identified a feedback loop between gankyrin, an oncoprotein overexpressed in human HCC, and Nrf2 maintaining the homeostasis in HCC cells. Mechanistically, gankyrin was found to interact with the Kelch domain of Keap1 and effectively competed with Nrf2 for Keap1 binding. Increased expression of gankyrin in HCC cells blocked the binding between Nrf2 and Keap1, inhibiting the degradation of Nrf2 by proteasome. Interestingly, accumulation and translocation of Nrf2 increased the transcription of gankyrin through binding to the ARE elements in the promoter of gankyrin. The positive feedback regulation involving gankyrin and Nrf2 modulates a series of antioxidant enzymes, thereby lowering intracellular ROS and conferring a steadier intracellular environment, which prevents mitochondrial damage and cell death induced by excessive oxidative stress. Our results indicate that gankyrin is a regulator of cellular redox homeostasis and provide a link between oxidative stress and the development of HCC.

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