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Reactive oxygen species from mitochondria mediate SW480 cells apoptosis induced by Na2SeO3
Hai-Tao Wang1, Xiang-Liang Yang, Zhi-Hong Zhang
1Department of Chemistry, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Abstract:
A number of selenium compounds have been found to inhibit tumorigenesis in a variety of animal and cell models. In order to explore the molecular mechanism involved in the anticarcinogenesis activity of selenium, we examined the effects of sodium selenite on cell viabilty, generation of reactive oxygen species (ROS), and mitochondrial transmembrane potential (delta(psi)m) in human colonic carcinoma cells SW480. The result from MTT test showed that sodium selenite reduced cell viability. Morophologic and flow cytometric results indicated that Na2SeO3 induced the apoptosis of SW480 cells. Na2SeO3 increased the generation of intracellular ROS, whereas BAPTA-AM, rotenone, and NaCN completely inhibited the increase of ROS induced by Na2SeO3. Na2SeO3 also caused the disruption of delta(psi)m. The intracellular ROS increase and apoptosis induced by Na2SeO3 were significantly decreased by superoxide dismutase (SOD), catalase. These data suggest that the ROS mediate apoptosis induced by Na2SeO3 and mitochondria may be a major source of Na2SeO3-induced ROS.
Insights
Sodium selenite induces apoptosis in human colon cancer cells by increasing reactive oxygen species (ROS) and disrupting mitochondrial potential. Antioxidants like SOD and catalase mitigate these effects, suggesting ROS mediation.
Area of Science:
- Cell Biology
- Biochemistry
- Toxicology
Background:
- Selenium compounds, including sodium selenite, show potential in inhibiting cancer development.
- Understanding the molecular mechanisms of selenium's anticarcinogenic effects is crucial for therapeutic development.
Purpose of the Study:
- To investigate the effects of sodium selenite on human colonic carcinoma cells (SW480).
- To elucidate the role of reactive oxygen species (ROS) and mitochondrial function in sodium selenite-induced apoptosis.
Main Methods:
- MTT assay to assess cell viability.
- Morphological analysis and flow cytometry to detect apoptosis.
- Measurement of intracellular ROS generation and mitochondrial transmembrane potential (Δψm).
- Use of ROS inhibitors (BAPTA-AM, rotenone, NaCN) and antioxidants (superoxide dismutase, catalase).
Main Results:
- Sodium selenite significantly reduced SW480 cell viability.
- Sodium selenite induced apoptosis in SW480 cells.
- Sodium selenite increased intracellular ROS generation and disrupted mitochondrial transmembrane potential.
- The increase in ROS and apoptosis induced by sodium selenite were attenuated by superoxide dismutase and catalase.
Conclusions:
- Reactive oxygen species (ROS) mediate the apoptosis induced by sodium selenite in SW480 cells.
- Mitochondria appear to be a primary source of ROS generated by sodium selenite.
- Sodium selenite exhibits anticancer properties through ROS-mediated apoptosis involving mitochondrial pathways.