Improvements in screening strategies and novel antitumor drugs promote longer survival of cancer patients, but many drugs also have serious side effects including both short-term and long-term brain injury. Oxidative stress (OS) is the major effect of antitumor drug-induced cognitive impairment and is caused by an imbalance between reactive oxygen species (ROS) and endogenous antioxidants in response to injury, leading to brain injury.

Though the role of oxidative stress in anti-tumor drug-induced brain injury has been identified, prevention strategies have been far from successful. Many studies describe antitumor drug therapy for brain injury, including methotrexate, natural plant extracts, animal extracts, or chemically synthesized artificial antioxidants. The success of animal modeling in various drug efficacy studies does not translate well in humans and, even if it did, large-scale clinical trials are lacking.

The aim of this Special Issue is to summarize the present knowledge of oxidative stress in antitumor drug-induced brain injury including cell molecular mechanisms, prevention and treatment strategies, drug research, and population experiments. Original research and review articles are welcome.

Potential topics include but are not limited to the following:

• The prevention of oxidative stress induced by anti-tumor drugs
• Subcellular organelle damage in anti-tumor drug-induced oxidative stress
• Dysregulation of protein regulation in anti-tumor drug-induced oxidative stress
• Role of nitric oxide synthase in anti-tumor drug-induced brain injury
• Role of NADPH oxidase in anti-tumor drug-induced brain injury
• The prevention of oxidative stress induced by radiotherapy drugs
• Subcellular organelle damage in radiotherapy-induced oxidative stress
• Dysregulation of protein regulation in radiotherapy-induced oxidative stress
• Role of nitric oxide synthase in radiotherapy-induced brain injury
• Role of NADPH oxidase inradiotherapy-induced brain injury