Oxidative Stress, Mitochondrial Dysfunction, and Neurotoxicity
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: 10 November 2024 | Viewed by 60
Special Issue Editor
Interests: antioxidants; oxidative stress; molecular mechanism; autophagy; ferroptosis; neurotoxicity
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Neurotoxicity could be induced by various drugs and environmental compounds, including antibacterial drugs (e.g., colistin, cefepime), anticancer drugs (e.g., paclitaxel, bortezomib, cisplatin), heavy metals (e.g., cadmium, copper, lead) and pathogenic toxins (e.g., lipopolysaccharide [LPS], T-2 toxin, deoxynivalenol), resulting in the development of irreversible neurodegeneration or even death in humans and animals. An understanding of the precise molecular mechanisms is required for the development of effective protective agents and novel therapeutic strategies for these drugs or toxin-induced neurotoxicity. Cellular oxidative stress is a consequence of an imbalance between the generation and detoxification of reactive oxygen species (ROS). Recent studies indicated that oxidative stress is involved in multiple cell death processes, including autophagic, ferroptotic and cuproptotic cell deaths. 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 products and targets of cellular ROS. Oxidative stress usually causes mitochondrial dysfunction, and they are often implicated during neurotoxicity and neurological disease, 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 drug- or toxin-induced neurotoxicity. The previous issue: Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction.
We look forward to receiving your contributions.
Dr. Chongshan Dai
Guest Editor
Manuscript Submission Information
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Keywords
- oxidative stress
- mitochondrial dysfunction
- neurotoxicity
- molecular mechanism
- neuroprotective agents
