scholarly journals Promoting effects of monomethylarsonic acid, dimethylarsinic acid and trimethylarsine oxide on induction of rat liver preneoplastic glutathione S-transferase placental form positive foci: A possible reactive oxygen species mechanism

2002 ◽  
Vol 100 (2) ◽  
pp. 136-139 ◽  
Author(s):  
Takayuki Nishikawa ◽  
Hideki Wanibuchi ◽  
Motome Ogawa ◽  
Anna Kinoshita ◽  
Keiichirou Morimura ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Rat Liver ◽  
Reactive Oxygen ◽  
Dimethylarsinic Acid ◽  
Oxygen Species ◽  
Glutathione S Transferase ◽  
Monomethylarsonic Acid ◽  
Trimethylarsine Oxide

scholarly journals Long-Term Alteration of Reactive Oxygen Species Led to Multidrug Resistance in MCF-7 Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Juan Cen ◽  
Li Zhang ◽  
Fangfang Liu ◽  
Feng Zhang ◽  
Bian-Sheng Ji
Keyword(s):  
Reactive Oxygen Species ◽  
Multidrug Resistance ◽  
Hypoxia Inducible Factor ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Related Factor ◽  
Oxygen Species ◽  
Glutathione S Transferase ◽  
Mcf 7

Reactive oxygen species (ROS) play an important role in multidrug resistance (MDR). This study aimed to investigate the effects of long-term ROS alteration on MDR in MCF-7 cells and to explore its underlying mechanism. Our study showed both long-term treatments of H2O2 and glutathione (GSH) led to MDR with suppressed iROS levels in MCF-7 cells. Moreover, the MDR cells induced by 0.1 μM H2O2 treatment for 20 weeks (MCF-7/ROS cells) had a higher viability and proliferative ability than the control MCF-7 cells. MCF-7/ROS cells also showed higher activity or content of intracellular antioxidants like glutathione peroxidase (GPx), GSH, superoxide dismutase (SOD), and catalase (CAT). Importantly, MCF-7/ROS cells were characterized by overexpression of MDR-related protein 1 (MRP1) and P-glycoprotein (P-gp), as well as their regulators NF-E2-related factor 2 (Nrf2), hypoxia-inducible factor 1 (HIF-1α), and the activation of PI3K/Akt pathway in upstream. Moreover, several typical MDR mediators, including glutathione S-transferase-π (GST-π) and c-Myc and Protein Kinase Cα (PKCα), were also found to be upregulated in MCF-7/ROS cells. Collectively, our results suggest that ROS may be critical in the generation of MDR, which may provide new insights into understanding of mechanisms of MDR.

Impact of Sodium Arsenite on Chromosomal Aberrations With Respect to Polymorphisms of Detoxification and DNA Repair Genes

2014 ◽  
Vol 33 (6) ◽  
pp. 518-522 ◽  
Author(s):  
Fatemeh Azizian-Farsani ◽  
Gholamreza Rafiei ◽  
Mostafa Saadat
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Repair ◽  
Chromosomal Aberrations ◽  
Sodium Arsenite ◽  
Reactive Oxygen ◽  
Final Concentration ◽  
Dna Repair Genes ◽  
Oxygen Species ◽  
Glutathione S Transferase ◽  
Repair Genes

Arsenic compounds can increase production of reactive oxygen species. Reactive oxygen species can induce double-strand breaks in DNA, which is a cause of chromosome aberrations (CAs). This study was conducted to determine the association between arsenic exposure and polymorphisms of genes involved in detoxification (glutathione S-transferase T1 [ GSTT1], glutathione S-transferase M1 [ GSTM1], glutathione S-transferase O2 [ GSTO2], catalase [ CAT], and NAD(P)H quinone oxidoreductase1 [ NQO1]) as well as nonhomologous end joining DNA repair genes ( XRCC4, XRCC5, and XRCC6) with induction of chromosomal aberrations. The participants consisted of 123 healthy males who were genotyped using polymerase chain reaction-based methods. Primary cultures of whole blood were treated with sodium arsenite (NaAsO2; iAs(III); at final concentration 1 µmol/L), mitomycin C (at final concentration 60 ηg/mL; as positive control), or untreated. For each culture, mitotic index (MI), chromatid breaks (CBs), CAs, and total percentage of aberrant cells were determined. The levels of CB and percentage of aberrant cells were significantly higher in the TT genotype of CAT (C-262T polymorphism) than the CC genotype. The CB value in samples with GSTM1 active genotype was significantly higher than the null genotype. The MI in samples with TT genotype of NQO1 (C609T polymorphism) was significantly higher than MI in samples having CC and CT genotypes. There was no association between MI, CB, CA, and percentage of aberrant cells and polymorphisms of XRCC4, XRCC5, and XRCC6.

scholarly journals Glutathione S-transferase A2 (GSTA2) Promotes Hepatocellular Carcinoma Recurrence After Liver Transplantation Through Modulating Reactive Oxygen Species Metabolism

2020 ◽  
Author(s):  
Kevin Tak-Pan NG ◽  
Oscar Wai-Ho Yeung ◽  
Yin Fan Lam ◽  
Jiang Liu ◽  
Hui Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Reactive Oxygen Species ◽  
Liver Transplantation ◽  
Early Phase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Glutathione S Transferase ◽  
Proliferation And Metastasis ◽  
Hcc Recurrence ◽  
Hcc Cells

Abstract BackgroundAn inevitable hepatic injury at the early phase after liver transplantation vitally affects the late phase hepatocellular carcinoma (HCC) recurrence. However, their linkage and underlying risk factors of HCC recurrence are unclear. This study aimed to clarify the clinical impact and functional roles of glutathione S-transferase A2 (GSTA2) in affecting HCC recurrence after liver transplantation.MethodsExpression significance and prognostic value of hepatic and circulating GSTA2 in HCC recipients were examined. The polymorphism of GSTA2 transcript was analysed by Sanger sequencing. The functions and molecular mechanisms of GSTA2 in the proliferation and metastasis of HCC were characterized by molecular, cellular and animal experiments. ResultsThe GSTA2 expression was significantly correlated with the early phase hepatic and systemic injury and reactive oxygen species (ROS) level after liver transplantation. Importantly, the level of the early phase circulating GSTA2 protein was a significant predictor of HCC recurrence and survival of HCC recipients. Heterogeneous single nucleotide polymorphism at G335C of GSTA2 was significantly associated with poor survival of HCC recipients. The GSTA2 expression was positively correlated with the aggressiveness of HCCs. Overexpression of GSTA2, by endogenous or exogenous approaches, could enhance the proliferation and invasion of HCCs through activating epithelial-mesenchymal-transition promoting proteins. Targeted inhibition of GSTA2 remarkably suppressed the proliferation and metastasis of HCCs. Increased level of GSTA2 could compensate the H2O2-induced ROS stress and therefore protect the HCC cells from damage. Alteration of GSTA2 expression in HCC cells could influence the activation of ROS-associated JNK and AKT signaling pathways and the expression of ROS-associated genes in responding to the H2O2 condition. ConclusionsOur research discovered GSTA2 to be the significant risk factor of HCC recurrence via providing a favorable ROS environment for HCC to survival and progress. This study presents a novel functional biomarker for combating HCC recurrence after liver transplantation.

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