MECHANISM OF CAPSEBON NANOPARTICLES INDUCED OXIDATIVE STRESS AND APOPTOSIS IN Caco-2 CELLS

Capsebon (CdS) nanoparticles are extensively used in excipients, drugs and paints, plastics, textiles, ceramic and glass industry. The high exposure to capsebon nanoparticles causes adverse effect on skin, eyes, respiratory track and kidney. The toxicity profile of capsebon nanoparticles on human colon cancer (Caco-2) cells is not finally understood. Hence, in this study capsebon nanoparticles were characterized were characterized by UV-visible spectrophotometer, dynamic light scattering and transmission electron microscope. The cell toxicity of capsebon nanoparticles was observed in Caco-2 cells by using NRU and MTT tests. The percentage of cell death was increased as the dose and time of capsebon nanoparticles exposure was increased. The hike in the production of reactive oxygen species (ROS) in Caco-2 cells due to capsebon nanoparticles was checked by applying fluorescent dye DCFDA and production of ROS was time and dose dependent. The toxicity of capsebon nanoparticles in Caco-2 cells was correlated with the generation of ROS, compromisation of mitochondrial trans membrane potential (MTP) and nucleic acid damage. Thus the current observation was confirmed that mitochondria play an important role in genotoxicity and cytotoxicity induced capsebon nanoparticles in Caco-2 cells. Also, we have examined the oxidative stress biomarkers lipid peroxide (LPO), and glutathione (GSH) and LPO was increased and GSH was decreased in Caco-2 cells. In this experiment, we noticed that capsebon nanoparticles are more dangerous at higher dose and increased time. This work deals the dose and dependent cell toxicity and apoptosis in Caco-2 cells.