Tiron, a ROS scavenger, protects human lung cancer Calu-6 cells against antimycin A-induced cell death
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1Department of Physiology, Medical School, Institute for Medical Sciences, Chonbuk National University, JeonJu 561-180, Korea.
Abstract:
Antimycin A (AMA) inhibits the mitochondrial electron transport between cytochromes b and c. However, the relationship between AMA and lung cancer cells is poorly understood. In this study, we investigated the involvement of reactive oxygen species (ROS) and glutathione (GSH) in AMA-treated lung cancer Calu-6 cell death. Treatment with AMA reduced cell viability in a dose-dependent manner for 72 h. The intracellular ROS levels were decreased in Calu-6 cells treated with low doses of AMA (10, 25 or 50 microM) at 72 h. However, the levels increased in cells treated with a high dose of 100 microM AMA. Levels of O2.- were significantly increased in AMA-treated cells at 72 h. The increases in ROS levels including O2.- in AMA-treated cells were observed within 10 min. Treatment with AMA reduced the intracellular GSH content. SOD activity was up-regulated in AMA-treated Calu-6 cells at 72 h. However, catalase activity was down-regulated by AMA. Treatment with tiron, a ROS scavenger, reduced the intracellular ROS levels, which were associated with a partial reduction of apoptosis. Treatment with exogenous SOD and catalase significantly inhibited loss of the mitochondrial transmembrane potential (DeltaPsim) in AMA-treated Calu-6 cells. In conclusion, our results suggest that the changes of intracellular ROS and GSH affect apoptosis in AMA-treated Calu-6 cells.
Insights
Antimycin A (AMA) affects lung cancer cell death by altering reactive oxygen species (ROS) and glutathione (GSH). High AMA doses increase ROS, impacting cell viability and apoptosis.
Area of Science:
- Biochemistry
- Cell Biology
- Cancer Research
Background:
- Antimycin A (AMA) is known to inhibit mitochondrial electron transport.
- The precise mechanisms by which AMA affects lung cancer cells, particularly concerning oxidative stress, remain unclear.
Purpose of the Study:
- To investigate the roles of reactive oxygen species (ROS) and glutathione (GSH) in Antimycin A-induced cell death in Calu-6 lung cancer cells.
Main Methods:
- Calu-6 cells were treated with varying doses of AMA.
- Intracellular ROS levels, superoxide anion (O2.-) production, GSH content, SOD and catalase activities were measured.
- Apoptosis and mitochondrial membrane potential (ΔPsim) were assessed using ROS scavengers and exogenous enzymes.
Main Results:
- AMA reduced cell viability in a dose-dependent manner.
- Low AMA doses decreased ROS, while high doses increased ROS and O2.- levels.
- AMA treatment depleted intracellular GSH and altered SOD and catalase activities.
- ROS scavenging partially reduced apoptosis, and exogenous SOD/catalase protected mitochondrial potential.
Conclusions:
- Changes in intracellular ROS and GSH levels are critical mediators of apoptosis in AMA-treated Calu-6 lung cancer cells.
- AMA's effect on lung cancer cells involves complex modulation of oxidative stress pathways.
