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.
Intracellular reactive oxygen species are required for directional migration of resident and bone marrow-derived hepatic pro-fibrogenic cells
