scholarly journals 159 A Crucial Role of Nox2-Derived Reactive Oxygen Species in Ageing-Associated Metabolic Disorders and Brain Oxidative Damage

Heart ◽  
2016 ◽  
Vol 102 (Suppl 6) ◽  
pp. A114.1-A114
Author(s):  
Li Geng ◽  
Jian-Mei Li
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Crucial Role ◽  
Metabolic Disorders ◽  
Reactive Oxygen ◽  
Oxygen Species

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.

Crucial role of reactive oxygen species (ROS) for the proapoptotic effects of indirubin derivative DKP-073 in melanoma cells

2018 ◽  
Vol 58 (2) ◽  
pp. 258-269 ◽  
Author(s):  
Veselina Zhivkova ◽  
Felix Kiecker ◽  
Peter Langer ◽  
Jürgen Eberle
Keyword(s):  
Reactive Oxygen Species ◽  
Crucial Role ◽  
Reactive Oxygen ◽  
Melanoma Cells ◽  
Oxygen Species

The role of reactive oxygen species in the hearts of dystrophin-deficient mdx mice

2007 ◽  
Vol 293 (3) ◽  
pp. H1969-H1977 ◽  
Author(s):  
Iwan A. Williams ◽  
David G. Allen
Keyword(s):  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Collagen Type ◽  
Reactive Oxygen ◽  
Mdx Mice ◽  
Oxygen Species ◽  
Collagen Type Iii ◽  
Fractional Shortening

Duchenne muscular dystrophy (DMD) is caused by deficiency of the cytoskeletal protein dystrophin. Oxidative stress is thought to contribute to the skeletal muscle damage in DMD; however, little is known about the role of oxidative damage in the pathogenesis of the heart failure that occurs in DMD patients. The dystrophin-deficient ( mdx) mouse is an animal model of DMD that also lacks dystrophin. The current study investigates the role of the antioxidant N-acetylcysteine (NAC) on mdx cardiomyocyte function, Ca2+ handling, and the cardiac inflammatory response. Treated mice received 1% NAC in their drinking water for 6 wk. NAC had no effect on wild-type (WT) mice. Immunohistochemistry experiments revealed that mdx mice had increased dihydroethidine (DHE) staining, an indicator of superoxide production; NAC-treatment reduced DHE staining in mdx hearts. NAC treatment attenuated abnormalities in mdx cardiomyocyte Ca2+ handling. Mdx cardiomyocytes had decreased fractional shortening and decreased Ca2+ sensitivity; NAC treatment returned mdx fractional shortening to WT values but did not affect the Ca2+ sensitivity. Immunohistochemistry experiments revealed that mdx hearts had increased levels of collagen type III and the macrophage-specific protein, CD68; NAC-treatment returned collagen type III and CD68 expression close to WT values. Finally, mdx hearts had increased NADPH oxidase activity, suggesting it could be a possible source of increased reactive oxygen species in mdx mice. This study is the first to demonstrate that oxidative damage may be involved in the pathogenesis of the heart failure that occurs in mdx mice. Therapies designed to reduce oxidative damage might be beneficial to DMD patients with heart failure.

Oxidative Stress and Cancer

2019 ◽  
Vol 24 (40) ◽  
pp. 4771-4778 ◽  
Author(s):  
James E. Klaunig
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Oxidative Damage ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Genetic Inheritance

Background: Cancer is considered a major cause of death worldwide. The etiology of cancer is linked to environmental and genetic inheritance causes. Approximately 90 percent of all human cancers have an environmental cause (non-genetic inheritance) predominantly through lifestyle choices (smoking, diet, UV radiation) while the remaining due to infections and chemical exposure. Cancer is a multistage process that involves mutational changes and uncontrolled cell proliferation. Research has firmly established a causal and contributory role of oxidative stress and oxidative damage in cancer initiation and progression. Methods: The purpose of this article is to review the role that oxidative stress and reactive oxygen species play in the development of cancer. Both endogenous and exogenous sources of reactive oxygen species result in increased oxidative stress in the cell. Excess reactive oxygen fumed can result in damage to and modification of cellular macromolecules most importantly genomic DNA that can produce mutations. In addition, oxidative stress modulates gene expression of downstream targets involved in DNA repair, cell proliferation and antioxidants. The modulation of gene expression by oxidative stress occurs in part through activation or inhibition of transcription factors and second messengers. The role of single nuclear polymorphism for oxidative DNA repair and enzymatic antioxidants is important in determining the potential human cancer risk. Conclusion: oxidative stress and the resulting oxidative damage are important contributors to the formation and progression of cancer.

Sign in / Sign up

Export Citation Format

Share Document