scholarly journals Role of Reactive Oxygen Species-elicited Apoptosis in the Pathophysiology of Mitochondrial and Neurodegenerative Diseases Associated With Mitochondrial DNA Mutations

2009 ◽  
Vol 108 (8) ◽  
pp. 599-611 ◽  
Author(s):  
Chun-Yi Liu ◽  
Cheng-Feng Lee ◽  
Yau-Huei Wei
2019 ◽  
Vol 7 (39) ◽  
pp. 5947-5955
Author(s):  
Chien-Hui Su ◽  
Jyun-Wei Chen ◽  
Li-Da Chen ◽  
Jui-Chih Chang ◽  
Chin-San Liu ◽  
...  

Mitochondrial localization photosensitizer NV-12P may recognize 8-oxo-dG with PET and FRET mechanism. Furthermore, NV-12P can generate a reactive oxygen species to degrade 8-oxo-dG using a similar mechanism of methyl blue.


2011 ◽  
Vol 43 (1) ◽  
pp. 25-29 ◽  
Author(s):  
R. A. P. Costa ◽  
C. D. Romagna ◽  
J. L. Pereira ◽  
N. C. Souza-Pinto

2018 ◽  
Vol 19 (11) ◽  
pp. 3362 ◽  
Author(s):  
Landon Rohowetz ◽  
Jacob Kraus ◽  
Peter Koulen

The significance of oxidative stress in the development of chronic neurodegenerative diseases of the retina has become increasingly apparent in recent years. Reactive oxygen species (ROS) are free radicals produced at low levels as a result of normal cellular metabolism that are ultimately metabolized and detoxified by endogenous and exogenous mechanisms. In the presence of oxidative cellular stress, ROS are produced in excess, resulting in cellular injury and death and ultimately leading to tissue and organ dysfunction. Recent studies have investigated the role of excess ROS in the pathogenesis and development of chronic neurodegenerative diseases of the retina including glaucoma, diabetic retinopathy, and age-related macular degeneration. Findings from these studies are promising insofar as they provide clear rationales for innovative treatment and prevention strategies of these prevalent and disabling diseases where currently therapeutic options are limited. Here, we briefly outline recent developments that have contributed to our understanding of the role of ROS in the pathogenesis of chronic neurodegenerative diseases of the retina. We then examine and analyze the peer-reviewed evidence in support of ROS as targets for therapy development in the area of chronic neurodegeneration of the retina.


2005 ◽  
Vol 51 (3) ◽  
pp. 385-393 ◽  
Author(s):  
Saori Kawamura ◽  
Daisaku Takai ◽  
Keiko Watanabe ◽  
Jun-ichi Hayashi ◽  
Kazushige Hayakawa ◽  
...  

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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