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Updated: Sep 20, 2026

Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors
Published on: February 7, 2018
[Research progress on oxidative stress and apoptosis]
Qilong Chu1, Kedi Yang, Aiguo Wang
1School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Abstract:
Many research findings revealed that oxidative stress may induce apoptosis. At present, the explanations for this phenomenon are: 1) ROS activated nuclear factor-KB and induction of the expression of nuclear factor-KB; 2) mitochondria-mediated cell apoptosis; 3) ROS mediated DNA damage and P53 activation; 4) ROS activated SAPK pathway to apoptosis. In this paper, the progress on oxidative stress and apoptosis was reviewed.
Insights
Oxidative stress, an imbalance of reactive oxygen species (ROS), can trigger programmed cell death (apoptosis). This review covers key mechanisms linking ROS to apoptosis, including NF-κB activation and DNA damage.
Area of Science:
- Biochemistry
- Cell Biology
- Molecular Biology
Context:
- Oxidative stress is implicated in numerous diseases.
- Understanding the link between oxidative stress and apoptosis is crucial for therapeutic development.
Purpose:
- To review the current understanding of how oxidative stress induces apoptosis.
- To summarize the molecular mechanisms involved in ROS-mediated apoptosis.
Summary:
- Reactive oxygen species (ROS) can induce apoptosis through several pathways.
- Mechanisms include activation of nuclear factor-kappa B (NF-κB), mitochondrial dysfunction, DNA damage leading to P53 activation, and activation of the stress-activated protein kinase (SAPK) pathway.
Impact:
- Provides a consolidated overview of oxidative stress and apoptosis research.
- Highlights key molecular players and pathways for potential therapeutic targeting.
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