Effect and Mechanism of Benzyl Isothiocyanate on Active Oxygen Induced in Human Malignant Glioma U-87 MG Cell Line

OBJECTIVE To investigate the effect and mechanism of benzyl isothiocyanate(BITC) on active oxygen induced in human malignant glioma cell line U-87 MG. METHODS U-87 MG was dealed with BITC, MTS assay was employed to determine the effect of BITC on the proliferation of cancer cells. After 2 and 5 μmol·L^?1 U-87 MG cells was treatment with BITC, the alteration of intracellular ROS was measured by flow cytometry, the level of GSH, the activities change of complex III of the mitochondrial respiratory chain, the superoxide dismutase(SOD) and the quinine reductase(QR) was measured by biochemistry assay, the phosphorylation of p38-MAPK was measured by Western blotting assay and the transcriptional activities ARE was determined by reporter gene system. RESULTS BITC significantly inhibited the proliferation of U-87 MG with an IC50 of 15.2 μmol·L^?1. After 2 and 5 μmol·L^?1 BITC treatment for 24 h, intracellular ROS was 376.3% and 607.5%(P<0.05), while the level of GSH was 71.3% and 44.9%(P<0.05), the level of SOD was 63.5% and 21.8%(P<0.05), the level of QR was 55.2% and 26.7%(P<0.05) and level of complex III was 48.5% and 37.6%(P<0.05). Western blotting showed that the phosphorylation of p38-MAPK was upregulated and the transcriptional activities of ARE were 141.1% and 215.2%. CONCLUSION BITC can induce ROS elevation in the tumor cells and the mechanism may be the regulation of oxidative stress related gene expression.