scholarly journals Mechanism of protein oxidative damage that is coupled to long-range electron transfer to high-valent haems

2016 ◽  
Vol 473 (12) ◽  
pp. 1769-1775 ◽  
Author(s):  
Zhongxin Ma ◽  
Heather R. Williamson ◽  
Victor L. Davidson
Keyword(s):  
Reactive Oxygen Species ◽  
Electron Transfer ◽  
Oxidative Damage ◽  
Long Range ◽  
Direct Contact ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
High Valent

The present study describes how oxidative damage to a protein may occur without direct contact with a reactive oxygen species, and how that radical-mediated damage can be propagated through the protein. This process is coupled to the reactivity of high-valent haems within the same protein.

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.

scholarly journals Ultraendurance exercise increases the production of reactive oxygen species in isolated mitochondria from human skeletal muscle

2010 ◽  
Vol 108 (4) ◽  
pp. 780-787 ◽  
Author(s):  
Kent Sahlin ◽  
Irina G. Shabalina ◽  
C. Mikael Mattsson ◽  
Linda Bakkman ◽  
Maria Fernström ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Vastus Lateralis ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Work Intensity ◽  
Isolated Mitochondria ◽  
Mitochondrial Ros

Exercise-induced oxidative stress is important for the muscular adaptation to training but may also cause muscle damage. We hypothesized that prolonged exercise would increase mitochondrial production of reactive oxygen species (ROS) measured in vitro and that this correlates with oxidative damage. Eight male athletes (24–32 yr) performed ultraendurance exercise (kayaking/running/cycling) with an average work intensity of 55% V̇o2peak for 24 h. Muscle biopsies were taken from vastus lateralis before exercise, immediately after exercise, and after 28 h of recovery. The production of H2O2 was measured fluorometrically in isolated mitochondria with the Amplex red and peroxidase system. Succinate-supported mitochondrial H2O2 production was significantly increased after exercise (73% higher, P = 0.025) but restored to the initial level at recovery. Plasma level of free fatty acids (FFA) increased fourfold and exceeded 1.2 mmol/l during the last 6 h of exercise. Plasma FFA at the end of exercise was significantly correlated to mitochondrial ROS production ( r = 0.74, P < 0.05). Mitochondrial content of 4-hydroxy-nonenal-adducts (a marker of oxidative damage) was increased only after recovery and was not correlated with mitochondrial ROS production. Total thiol group level and glutathione peroxidase activity were elevated after recovery. In conclusion, ultraendurance exercise increases ROS production in isolated mitochondria, but this is reversed after 28 h recovery. Mitochondrial ROS production was not correlated with oxidative damage of mitochondrial proteins, which was increased at recovery but not immediately after exercise.

Loss of TRPML1 promotes production of reactive oxygen species: is oxidative damage a factor in mucolipidosis type IV?

2013 ◽  
Vol 457 (2) ◽  
pp. 361-368 ◽  
Author(s):  
Jessica Coblentz ◽  
Claudette St. Croix ◽  
Kirill Kiselyov
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Ion Channel ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mucolipidosis Type Iv ◽  
Type Iv ◽  
Mucolipidosis Type

TRPML1 is a lysosomal ion channel permeable to cations, including Fe2+. Our data suggest that TRPML1 redistributes Fe2+ between the lysosomes and the cytoplasm. Loss of TRPML1 leads to production of reactive oxygen species, and to mitochondrial deterioration.

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