Role of Oxidative Stress in Catecholamine-Induced Changes in Cardiac Sarcolemmal Ca2+ Transport

2001 ◽  
Vol 387 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Paramjit S. Tappia ◽  
Tomoji Hata ◽  
Lena Hozaima ◽  
Manjot S. Sandhu ◽  
Vincenzo Panagia ◽  
...  
2004 ◽  
Vol 6 (5) ◽  
pp. 914-923 ◽  
Author(s):  
Petr Ostadal ◽  
Adel B. Elmoselhi ◽  
Irena Zdobnicka ◽  
Anton Lukas ◽  
Vijayan Elimban ◽  
...  

2004 ◽  
Vol 6 (5) ◽  
pp. 914-923 ◽  
Author(s):  
Petr Ostadal ◽  
Adel B. Elmoselhi ◽  
Irena Zdobnicka ◽  
Anton Lukas ◽  
Vijayan Elimban ◽  
...  

2019 ◽  
Vol 18 (5) ◽  
pp. 372-381 ◽  
Author(s):  
Vikas Pareek ◽  
Banshi Nath ◽  
Prasun K. Roy

Background & Objective:Oxidative stress (OS) is the secondary source of an injury in consequence to the earlier caused primary injury; it is the condition of an imbalance between oxidants and antioxidants within the physiological system. OS causes alterations in proteins and DNA structure, leading to inflammation, apoptotic cell death, and tissue damage. Neurodegenerative diseases (NDDs) such as Alzheimer's disease, Parkinson's disease, Glioma-induced neurodegeneration and the normal aging-related neuro-degeneration are primarily associated with the increased OS. The present review article is committed to delivering a comprehensive overview of the current neuroimaging modalities which estimates an indirect correlate of OS in the brain. OS-induced changes in white matter tracts and the gray matter volumes are reviewed assessing the role of diffusion tensor imaging (DTI) and voxel-based morphometry (VBM) respectively. Further, the role of magnetic resonance spectroscopy (MRS) to assess the OS-induced alterations of chemical moieties, and thus the resultant structural implications in the neurological disorders are also briefly as well as precisely reviewed.Conclusions:In the present review article we present an overview of the role of neuroimaging modalities in the diagnosis, and longitudinal assessment during treatment of the OS induced changes.


2007 ◽  
Vol 293 (6) ◽  
pp. H3524-H3531 ◽  
Author(s):  
Sanjiv Dhingra ◽  
Anita K. Sharma ◽  
Dinender K. Singla ◽  
Pawan K. Singal

It is known that TNF-α increases the production of ROS and decreases antioxidant enzymes, resulting in an increase in oxidative stress. IL-10 appears to modulate these effects. The present study investigated the role of p38 and ERK1/2 MAPKs in mediating the interplay of TNF-α and IL-10 in regulating oxidative stress and cardiac myocyte apoptosis in Sprague-Dawley male rats. Isolated adult cardiac myocytes were exposed to TNF-α (10 ng/ml), IL-10 (10 ng/ml), and IL-10 + TNF-α ( ratio 1) for 4 h. H2O2(100 μM) as a positive control and the antioxidant Trolox (20 μmol/l) were used to confirm the involvement of oxidative stress. H2O2treatment increased oxidative stress and apoptosis; TNF-α mimicked these effects. Exposure to TNF-α significantly increased ROS production, caused cell injury, and increased the number of apoptotic cells and Bax-to-Bcl-xl ratio. This change was associated with an increase in the phospho-p38 MAPK-to-total p38 MAPK ratio and a decrease in the phospho-ERK1/2-to-total ERK1/2 ratio. IL-10 treatment by itself had no effect on these parameters, but it prevented the above-listed changes caused by TNF-α. The antioxidant Trolox modulated TNF-α-induced changes in Bax/Bcl-xl, cell injury, and MAPKs. Preexposure of cells to the p38 MAPK inhibitor SB-203580 prevented TNF-α-induced changes. Inhibition of the ERK pathway with PD-98059 attenuated the protective role of IL-10 against TNF-α-induced apoptosis. This study provides evidence in support of the essential role of p38 and ERK1/2 MAPKs in the interactive role of TNF-α and IL-10 in cardiac myocyte apoptosis.


2006 ◽  
Vol 21 (1) ◽  
pp. 42-47 ◽  
Author(s):  
Ahmet Ateşşahin ◽  
İzzet Karahan ◽  
Gaffari Türk ◽  
Seyfettin Gür ◽  
Seval Yılmaz ◽  
...  

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