Cytotoxicity and apoptosis effects of zno nanoparticles in human liver cancer cells (hepg2)

Nowadays, due to the widespread and severe psychological complications for cancer patients , there is a necessary need to extend new prevention and treatment methods of cancer disease. The mostimportant cancer characteristic is the ability of cancer cells to inhibit apoptosis and continue cells proliferation. Liver is the main organ of metabolism and liver cancer is also one of the commonmalignancies which has major impacts on the vital organs. Cancer treatment methods such as surgery, chemotherapy and radiotherapy have side effects and no effective results specially in advanced cancer. Todays the metal nanoparticles like ZnO are used to diagnose cancers. In a research that examined the mechanism of ZnO NPs cytotoxicity on human liver cancer (Hep G2) cells, results showed that use of ZnO NPs has distinct effect on the survival of mammalian cells through eliminating cancer cells. In HepG2 cells treated with ZnO NPs , Protection and mRNA levels of the tumour preventive gene (P53) and apoptotic gene (bax) were increased while the anti apoptotic gene (bcl2) was decreased. It also caused activity of caspase 3 enzyme, DNA fragmentation, reactive oxygen species and oxidative stress in HepG2 cells. In another study, HepG2 exposed to 14-20฀/ ฀ ZnO NPs for 12 h exhibited a reduced viability by inducing apoptosis. In additional reactive oxygen increased the bax/bcl2 ratio byreducing the mitochondrial membrane potential, which is responsible for inducing mitochondrial apoptosis. Also ZnONPs activated JNK, P53 pathways and induced P53 phosphorylation. Through apoptosis was not related to JNK and P38 pathways. In general ,it can be said that ZnO NPs selectively induced apoptosis in liver cancer cells by creating active oxygen through the P53 pathway such as the effect of anticancer drugs.

کلیدواژه ها:

Cancer Diagnosis ، Cancer Prevention ، Cell and Cancer ، Cancer Treatment and Management ، Drugs and Cancer