Aim: To investigate the cytotoxic effects of tamoxifen on the breast cancer cell line (MCF7). Methods:The cytotoxic effects of tamoxifen on MCF7 cells were investigated using caspase-9 activity and high content screening assays. Apoptosis mechanisms following tamoxifen treatment were also investigated. Results:The most significant cytotoxic effect of tamoxifen in MCF7 cells was a half-maximal inhibitory concentration (IC 50 ) of 4.506 µg/mL. A significant increase in caspase-9 activity was also observed when MCF7 cells were treated with tamoxifen (5 µg/mL). Furthermore, increased cell membrane permeability, cytochrome c level, and nuclear intensity were observed with tamoxifen (100 µg/mL) compared with doxorubicin (20 µg/mL) treatment. However, a noticeable decrease in cell viability and mitochondrial membrane permeability was observed with tamoxifen (100 µg/mL) treatment compared with doxorubicin (20 µg/mL) as a positive control. Conclusion:Tamoxifen showed in vitro cytotoxic effects in MCF7 cells as demonstrated by high-content screening and caspase-9 activity assays. Tamoxifen inhibits estrogen mechanisms, although toxic effect was observed.

Multipara metric analysis of compound toxicity at the level of individual cells using flow cytometry and cellular imaging-based approaches such as High Content Screening (HCS) have played key roles in the detection of toxicity and classification of compounds based on observed patterns of reversible and irreversible cellular injury. Gold III complex (AuL 2 ) of bidentate ligand derived from the cyclization reaction of Schiff base of 4-amino-5-phenyl-4h-1,2,4-triazole-3-thiol with thioglycolic acid was synthesized and characterized by using melting point, FTIR spectroscopy, 1 HNMR, UV-Visible spectroscopy and elemental analysis. The presence of chloride counter ion in complex was supported by conductivity measurement and the presence of hydrated water was supported by thermal gravimetric studies. We examine the cytotoxic effects of gold complex and its ligand in one cultured cellular models (MCF7 cell line) by High Content Screening (HCS) and analysis and cell viability assay (MMT assay). The inhibitory effect of AuL 2 on breast cancer cell growth was due to induction of apoptosis as evidenced by annexin V staining and cell shrinkage. The study found that AuL 2 -mediated lead to disruption of Mitochondrial Membrane Potential (MMP), cell membrane permeability, nuclear condensation, fragmentation and release of cytochrome c from the mitochondria into the cytosol and also suggesting AuL 2 as a potential MCF7 inhibitor compared to doxorubicin as positive control. In this study, data showed that gold (III) complex AuL 2 may have therapeutic value in breast cancer treatment worthy of further development.