Selective cytotoxicity of goniothalamin against hepatoblastoma HepG2 cells.

Liver cancer has become one of the major types of cancer with high mortality and liver cancer is not responsive to the current cytotoxic agents used in chemotherapy. The purpose of this study was to examine the in vitro cytotoxicity of goniothalamin on human hepatoblastoma HepG2 cells and normal liver Chang cells. The cytotoxicity of goniothalamin against HepG2 and liver Chang cell was tested using MTT cell viability assay, LDH leakage assay, cell cycle flow cytometry PI analysis, BrdU proliferation ELISA assay and trypan blue dye exclusion assay. Goniothalamin selectively inhibited HepG2 cells [IC50 = 4.6 (±0.23) µM in the MTT assay; IC50 = 5.20 (±0.01) µM for LDH assay at 72 hours], with less sensitivity in Chang cells [IC50 = 35.0 (±0.09) µM for MTT assay; IC50 = 32.5 (±0.04) µM for LDH assay at 72 hours]. In the trypan blue dye exclusion assay, the Viability Indexes were 52 ± 1.73% for HepG2 cells and 62 ± 4.36% for Chang cells at IC50 after 72 hours. Cytotoxicity of goniothalamin was related to inhibition of DNA synthesis, as revealed by the reduction of BrdU incorporation. At 72 hours, the lowest concentration of goniothalamin (2.3 µL) retained 97.6% of normal liver Chang cells proliferation while it reduced HepG2 cell proliferation to 19.8% as compared to control. Besides, goniothalamin caused accumulation of hypodiploid apoptosis and different degree of G2/M arrested as shown in cell cycle analysis by flow cytometry. Goniothalamin selectively killed liver cancer cell through suppression of proliferation and induction of apoptosis. These results suggest that goniothalamin shows potential cytotoxicity against hepatoblastoma HepG2 cells.

Exploring SOD1 Gene for the Detection of Fetal Down Syndrome.

OBJECTIVE: Fetal cells and circulating cellfree fetal DNA increases in the maternal circulation in women carrying trisomy 21 fetus. METHODS: We attempted the use of superoxide dismutase (SOD-1) gene, which is located at the Down Syndrome Critical Region, to overcome this situation for the prenatal screening of Down syndrome. The prospective of the gene using real-time quantitative polymerase chain reaction was explored. RESULTS: The level of SOD-1 sequences is significantly elevated in the third trimester normal pregnancies (mean = 11728 copies/µl) when compared to the second trimester (mean = 5705.6 copies/µl), (p<0.005) and non pregnant normal women (mean = 3580.2 copies/µl), (p<0.0001). Down syndrome pregnancies have the greatest elevation compared to all the three trimesters of normal singleton pregnancies and twin pregnancies, p<0.05. CONCLUSIONS: These data indicate that a quantitative analysis using a gene associated with a disorder could be used in screening for the prenatal diagnosis of fetal aneuploidies regardless of the sex of the fetus.