Abstract: Objective To investigate the toxic effects and mechanisms of silica nanoparticles on myocardial mitochondrial. Methods The Balb/c mice were intratracheally instilled with silica nanoparticles (40 nm) at three doses of 7, 21 and 35 mg/kg every three days for a total of 5 times. Control group was given the same volume of normal saline. The transmission electron microscope was used to observe the ultrastructure of myocardial mitochondria. By measuring the concentration of ATP，the effect of silica nanoparticles on the function of myocardial mitochondria was evaluated. Through the detection of the ability of anti O2-·in the myocardial tissue, the antioxidant capacity of mitochondria in cardiac muscle was evaluated. The expression levels of cytochrome coxidase subunit 1 (COX1) and succinate dehydrogenase subunit a (SDHA) were detected by Western blot assay. Results The results showed that silica nanoparticles at high dose can damage the structure of myocardial mitochondrial, which induced swelling of mitochondria， mitochondrial cristae disorder disappeared and even mitochondrial fusion. Silica nanoparticles (21 and 35 mg/kg) can induced the decrease in functions of mitochondria. Silica nanoparticles (7 and 21 mg/kg) can enhance the myocardial antioxidant capacity. But high dose of silica nanoparticles can induce the decrease in the myocardial antioxidant capacity. Silica nanoparticles (21 mg/kg) induced mitochondrial biosynthesis, but high dose of silica nanoparticles (35 mg/kg) inhibited mitochondrial biosynthesis. Conclusion Silica nanoparticles (35 mg/kg) can induce the production of O2-· and decrease the antioxidant capacity of mitochondria, which leads to the damage of the function and structure of the mitochondria and inhibits the mitochondria biosynthesis.

Key words: nanostructures, environmental exposure, toxicity tests, silica nanoparticles, myocardial mitochondrial, mitochondria biosynthesis