Objective: To explore the proliferation and apoptosis effects induced by sodium arsenite and arsenic trioxide on human hepatocyte L02 and provide evidence for the paradox effects of arsenic.
Methods: Human hepatocyte L02 was treated by a series of concentration of sodium arsenite or arsenic trioxide, respectively. Cytotoxicity were tested by MTT assay and colony formation assay, cellular apoptosis and cell cycle were detected by flow cytometry, chromosomal breakage were measured by micronucleus test and reactive oxygen species level and GSH contents were detected with commercial kits.
Results: With the increase of sodium arsenite or arsenic trioxide concentrations, cellular viability, colony formation rate and GSH contents decreased; inhibition of colony formation, cellular apoptotic rate, reactive oxygen species level and frequency of micronuclei increased, and dosed cells were both arrested in G2/M phase of cell cycle.
Conclusion: Both sodium arsenite and arsenic trioxide could induce oxidative stress in human hepatocyte L02 and result in chromosomal damage, apoptosis, cell cycle arrest and cellular proliferation inhibition, suggesting that oxidative stress induction might be the common molecular mechanism of malignant transformation induced by sodium arsenite and therapeutic effects exhibited by arsenic trioxide.