New Insight into the Role of Reactive Oxygen Species (ROS) in Cellular Signal-Transduction Processes

2015 ◽  
pp. 221-254 ◽  
Author(s):  
Eileen G. Russell ◽  
Thomas G. Cotter
Keyword(s):  
Reactive Oxygen Species ◽  
Signal Transduction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cellular Signal Transduction ◽  
Cellular Signal ◽  
Insight Into

Role of reactive oxygen species and Cr(VI) in Ras-mediated signal transduction

2004 ◽  
Vol 255 (1/2) ◽  
pp. 119-127 ◽  
Author(s):  
Suwei Wang ◽  
Stephen S. Leonard ◽  
Jianping Ye ◽  
Ning Gao ◽  
Liying Wang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Signal Transduction ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Protection of Mycobacterium tuberculosis from Reactive Oxygen Species Conferred by the mel2 Locus Impacts Persistence and Dissemination

2009 ◽  
Vol 77 (6) ◽  
pp. 2557-2567 ◽  
Author(s):  
Suat L. G. Cirillo ◽  
Selvakumar Subbian ◽  
Bing Chen ◽  
Torin R. Weisbrod ◽  
William R. Jacobs ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mycobacterium Tuberculosis ◽  
Bacterial Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Wild Type ◽  
Primary Mechanism ◽  
Insight Into ◽  
Increased Susceptibility

ABSTRACT Persistence of Mycobacterium tuberculosis in humans represents a major roadblock to elimination of tuberculosis. We describe identification of a locus in M. tuberculosis, mel2, that displays similarity to bacterial bioluminescent loci and plays an important role during persistence in mice. We constructed a deletion of the mel2 locus and found that the mutant displays increased susceptibility to reactive oxygen species (ROS). Upon infection of mice by aerosol the mutant grows normally until the persistent stage, where it does not persist as well as wild type. Histopathological analyses show that infection with the mel2 mutant results in reduced pathology and both CFU and histopathology indicate that dissemination of the mel2 mutant to the spleen is delayed. These data along with growth in activated macrophages and infection of Phox−/− and iNOS−/− mice and bone marrow-derived macrophages suggest that the primary mechanism by which mel2 affects pathogenesis is through its ability to confer resistance to ROS. These studies provide the first insight into the mechanism of action for this novel class of genes that are related to bioluminescence genes. The role of mel2 in resistance to ROS is important for persistence and dissemination of M. tuberculosis and suggests that homologues in other bacterial species are likely to play a role in pathogenesis.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

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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