Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction

Dear Colleagues,

Neurotoxicity can be induced by many drugs and environmental toxins, including antibacterial drugs (e.g., colistin, and cefepime), anticancer drugs (e.g., paclitaxel, bortezomib, and cisplatin), heavy metals (e.g., cadmium, copper, and lead), and pathogenic toxins (e.g., lipopolysaccharide [LPS], T-2 toxin, and deoxynivalenol), finally resulting in the development of irreversible neurodegeneration and even death in humans and animals. Understanding the precise molecular mechanisms involved in neurotoxicity is essential to the development of effective agents and novel therapeutic strategies for its treatment. Cellular oxidative stress is a consequence of an imbalance between the generation and detoxification of reactive oxygen species (ROS). The nervous tissue is highly vulnerable to oxidative damage due to its high energy demand, high oxygen consumption, and abundance of peroxidiable fatty acids. In addition, mitochondria, the ‘power plant’ of cells, are the main producer and target of cellular ROS. Oxidative stress usually causes mitochondrial dysfunction and, which is often implicated during neurotoxicity and neurological diseases, but effective mechanism-based therapies remain elusive.

Therefore, this Special Issue aims to collate innovative original research and review articles that reveal new pathogenic pathways, potential therapeutic strategies, and neuroprotective agents, particularly focusing on oxidative stress, mitochondrial dysfunction, and their crosstalk to clarify and ameliorate drugs- or toxin-induced neurotoxicity.

Dr. Chongshan Dai
Dr. Shusheng Tang
Guest Editors

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