In a previous study,the lanthanum citrate complex([LaCit2]3-) has been found to induce apoptosis in the human HeLa cervical cancer cell line.To clarify the mechanism,we carried out comparative proteomics analysis between treated and control cells.Differentially expressed proteins were separated electrophoretically and identified by MALDI-TOF/TOF tandem mass spectrometry.There were profound changes in 14 proteins related to mitochondrial function and oxidative stress,suggesting that mitochondrial dysfunction plays a key role in [LaCit2]3--induced apoptosis.This was confirmed by a decrease in the mitochondrial transmembrane potential,and increases in cytochrome c release and reactive oxygen species generation in [LaCit2]3--treated cells.Western blotting analyses show that [LaCit2]3--induced apoptosis was accompanied by the activation of caspase-9 and the specific proteolytic cleavage of PARP,leading to an increase in the proapoptotic protein Bax and a decrease in the antiapoptotic protein Bcl-2.These results suggest that [LaCit2]3-induced the apoptosis of HeLa cells through oxidative stress mediated pathway involving MT participation. In a previous study, the lanthanum citrate complex ([LaCit2] 3-) has been found to induce apoptosis in the human HeLa cervical cancer cell line. To clarify the mechanism, we carried out comparative proteomics analysis between treated and control cells. proteins were separated electrophoretically and identified by MALDI-TOF / TOF tandem mass spectrometry. There were profound changes in 14 proteins related to mitochondrial function and oxidative stress, suggesting that mitochondrial dysfunction plays a key role in [LaCit2] 3 - induced apoptosis. was confirmed by a decrease in the mitochondrial transmembrane potential, and increases in cytochrome c release and reactive oxygen species generation in [LaCit2] 3 - treated cells. Western blotting analyzes show that [LaCit2] 3 - induced apoptosis was accompanied by the activation of caspase-9 and the specific proteolytic cleavage of PARP, leading to an increase in the proapoptotic protein Bax and a decrease in the antiapoptotic protei n Bcl-2. These results suggest that [LaCit2] 3-induced the apoptosis of HeLa cells through oxidative stress mediated pathway involving MT participation.