EFFECT OF REACTIVE OXYGEN SPECIES ON APOPTOSISINDUCED BY Na_2SeO_3 IN SW480 CELLS
Wang Hai-tao
Abstract
Wang Hai-tao
Abstract
To investigate the mechanism of apoptosis induced by sodium selenite in a human colonic cancer cell line SW480. SW480 cells were loaded with fluorescent probes 2′,7′- DCFH-DA, and rhodamine123, respectively. The changes of intracellular ROS, and mitochondrial transmembrane potential (ΔΨm) was detected by using multiphoton imaging system. The results showed that (1) Na2SeO3 elevated SW480 cells apoptotic rate and intracellular ROS; SOD, catalase evidently suppressed ROS increase and reduced apoptotic rate, (2) Inhibition of mitochondrial electron transport with NaCN or rotenone almost blocked selenite-induced ROS production, (3) Na2SeO3 induced disruption of the mitochondrial transmembrane potential (ΔΨm). The data suggest that Na2SeO3 results in the increase intracellular ROS which origitesfrom mitochondia and mediates Na2SeO3-induced apoptosis.
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To investigate the mechanism of apoptosis induced by sodium selenite in a human colonic cancer cell line SW480. SW480 cells were loaded with fluorescent probes 2′,7′- DCFH-DA, and rhodamine123, respectively. The changes of intracellular ROS, and mitochondrial transmembrane potential (ΔΨm) was detected by using multiphoton imaging system. The results showed that (1) Na2SeO3 elevated SW480 cells apoptotic rate and intracellular ROS; SOD, catalase evidently suppressed ROS increase and reduced apoptotic rate, (2) Inhibition of mitochondrial electron transport with NaCN or rotenone almost blocked selenite-induced ROS production, (3) Na2SeO3 induced disruption of the mitochondrial transmembrane potential (ΔΨm). The data suggest that Na2SeO3 results in the increase intracellular ROS which origitesfrom mitochondia and mediates Na2SeO3-induced apoptosis.
Key concepts: Reactive oxygen species, Intracellular, Apoptosis, Chemistry, Membrane potential, Mitochondrion, Catalase, Cell biology