scholarly journals Role of Mitochondrial Dysfunction and Reactive Oxygen Species in Mediating Hypertension in the Reduced Uterine Perfusion Pressure Rat Model of Preeclampsia

Hypertension ◽  
2018 ◽  
Vol 72 (3) ◽  
pp. 703-711 ◽  
Author(s):  
Venkata Ramana Vaka ◽  
Kristen M. McMaster ◽  
Mark W. Cunningham ◽  
Tarek Ibrahim ◽  
Rebekah Hazlewood ◽  
...  
2008 ◽  
Vol 21 (10) ◽  
pp. 1152-1156 ◽  
Author(s):  
M. Sedeek ◽  
J. S. Gilbert ◽  
B. B. LaMarca ◽  
M. Sholook ◽  
D. L. Chandler ◽  
...  

2004 ◽  
Vol 27 (4) ◽  
pp. 228-233 ◽  
Author(s):  
Kamil Cam ◽  
Ferruh Simsek ◽  
Meral Yuksel ◽  
Levent Turker ◽  
Goncagul Haklar ◽  
...  

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.


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