Abstract
Limited understanding of mitochondria disorders that induced by nanoparticles is a stumbling block for anti-cancer drug delivery targeting strategy. In present study, C6 glioma cells were exposed to aminated and alkylated SiO&sub2; nanoparticles for mitochondrion disordering and cell metabolism study. Collective results showed that aminated nanoparticles tend to trigger the cell-repair mechanism in cancer cells while alkylated nanoparticles could cause irreversible damages on cancer cells, although both types of the particles were proved to damage mitochondrion. The underlying mechanism show that aminated nanoparticles induced proton-stuck effect in mitochondrion and self-repairing in cancer cells by up-regulating p21. Otherwise, alkylated nanoparticles damaged mitochondrion and induced phosphorylated cyclin E accumulation lead to Fbw7 down-regulation caused further S phase arrest and severe late apoptosis. This work can help us elucidate the mechanism of the clinic application of nano-drug carriers.