scholarly journals A Novel Technique for Harvesting Hepatic Vein Blood and Time Course of Posthepatic Reactive Oxygen Species after Liver Transplantation in Rats

2012 ◽  
Vol 01 (S1) ◽  
Author(s):  
Changku Jia ◽  
Youke Chen ◽  
Honglei Liu
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Transplantation ◽  
Hepatic Vein ◽  
Time Course ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Novel Technique

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.

Abstract 633: Aerobic Training Induces Time-course Changes Of Ace2-Ang(1-7)-Mas Receptor Axis And Reactive Oxygen Species In The Heart Of Spontaneously Hypertensive Rats

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Sebastião D Silva junior ◽  
Dulce E Casarini ◽  
Lisete C Michelini
Keyword(s):  
Reactive Oxygen Species ◽  
Time Course ◽  
Reactive Oxygen ◽  
Receptor Expression ◽  
Ros Production ◽  
Oxygen Species ◽  
Hypertensive Rats ◽  
Sequential Effects ◽  
Spontaneously Hypertensive ◽  
Mas Receptor

Objective: Since we showed recently that T causes time-dependent changes on brain RAS and oxidative stress of hypertensive rats, we sought now to investigate the sequential effects of T on ACE2-Ang(1-7)-MasR axis and reactive oxygen species (ROS) production in the left ventricle (LV) of SHRs. Methods: Male SHR and WKY aged 12 weeks underwent maximal exercise test (ET) and were allocated to T (50-60% of maximum exercise capacity, 1 h/day, 5 days/week) or sedentary (S) groups for 8 weeks. Subgroups of rats were cannulated at weeks 0 (S0), 1 (T1), 2 (T2), 4 (T4) and 8 (S8 and T8) for measurement of resting pressure (AP) and heart rate (HR), followed by saline perfusion and harvesting of the heart. ACE2 and MasR expression (Western Blotting) and ROS production (Dihydroethidium staining) were measured in the LV. Results: At the beginning of protocols SHR vs WKY exhibited higher MAP and HR (169±1 mmHg, 351±9 b/min, corresponding to 44% and 7% increases), elevated MasR (1,22±0,03 vs 1,00± 0,01 AU) but similar ACE2 expression (1,06±0,04 AU). ROS production was higher in SHR vs WKY (78±4 x 103 vs 66±1 x 103 AU). T increased treadmill performance (+0,87±0.10 km/h) and decreased resting HR (-15% at T4-T8) in both groups; MAP was only reduced in SHR (-10% at T8). T caused no change in the WKY group but increased ACE2 expression in the SHR (~1.14±0.03 au, T1-T4 P<0.05 vs WKY), with a biphasic response in Mas receptor expression: an early fall and a late increase (1,02±0,07 AU at T2-T4 and 1,20±0,04 AU at T8, respectively, P<0.05). In the SHR, T also caused an early normalization in ROS production (65±1 x 103 AU at T2) which was maintained up to T8. Again T did not change ROS production in the WKY group. Conclusions: Augmented ACE2 expression and reduced ROS production in the heart of the SHR are early responses to training, which are followed by a late increase in MasR expression. Data suggest that the prompt normalization of ROS production is mediated by ACE2-induced reduction of angiotensin II content in the LV of the trained SHR.

scholarly journals Chondrocyte cell death mediated by reactive oxygen species-dependent activation of PKC-βI

2006 ◽  
Vol 290 (3) ◽  
pp. C802-C811 ◽  
Author(s):  
Marcello DelCarlo ◽  
Richard F. Loeser
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cell Survival ◽  
Time Course ◽  
Reactive Oxygen ◽  
Specific Protein ◽  
Ros Production ◽  
Oxygen Species ◽  
Secondary Messenger ◽  
Promote Cell Survival

Signals generated by the extracellular matrix (ECM) promote cell survival. We have shown that chondrocytes detached from their native ECM and plated without serum at low density on poly-l-lysine undergo significant cell death that is associated with the production of reactive oxygen species (ROS). No cell death or ROS production was observed when cells were plated on fibronectin under the same conditions. Cell death on poly-l-lysine could be completely inhibited with the addition of either antioxidants or inhibitors of specific protein kinase C (PKC) isoforms including PKC-βI. PKC-βI was noted to translocate from the cytosol to the particulate membrane after plating on poly-l-lysine, and this translocation was inhibited by the addition of an antioxidant. Time-course analyses implicated endogenous ROS production as a secondary messenger leading to PKC-βI activation and subsequent chondrocyte cell death. Cell survival on poly-l-lysine was significantly improved in the presence of oligomycin or DIDS, suggesting that ROS production occurred via complex V of the electron transport chain of the mitochondria and that ROS were released to the cytosol via voltage-dependent anion channels. Together, these results represent a novel mechanism by which ROS can initiate cell death through the activation of PKC-βI.

Multifunctional UCNPs@MnSiO3@g-C3N4 nanoplatform: improved ROS generation and reduced glutathione levels for highly efficient photodynamic therapy

2017 ◽  
Vol 5 (12) ◽  
pp. 2456-2467 ◽  
Author(s):  
Lili Feng ◽  
Fei He ◽  
Yunlu Dai ◽  
Shili Gai ◽  
Chongna Zhong ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Photodynamic Therapy ◽  
Cancer Treatment ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Malignant Cells ◽  
Novel Technique ◽  
Highly Efficient

Photodynamic therapy (PDT) is a novel technique that has been extensively employed in cancer treatment; it utilizes reactive oxygen species to kill malignant cells.

Mitochondria as a source of reactive oxygen species

2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species
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