In vitro toxicity of silica nanoparticles in myocardial cells

Yiyi Ye; Jianwen Liu; Mingcang Chen; Lijuan Sun; Minbo Lan

doi:10.1016/j.etap.2009.12.002

In vitro toxicity of silica nanoparticles in myocardial cells

Environ Toxicol Pharmacol. 2010 Mar;29(2):131-7. doi: 10.1016/j.etap.2009.12.002. Epub 2009 Dec 28.

Authors

Yiyi Ye¹, Jianwen Liu, Mingcang Chen, Lijuan Sun, Minbo Lan

Affiliation

¹ State Key Laboratory of Bioreactor Engineering and School of Pharmacy, East China University of Science and Technology, 130 Meilong Road, Shanghai 200237, China.

PMID: 21787594
DOI: 10.1016/j.etap.2009.12.002

Abstract

In the present study, toxicities of silica nanoparticles with sizes of 21 and 48nm were assessed in myocardial H9c2(2-1) cells using the methylthiazolyldiphenyl-tetrazolium bromide reduction and lactate dehydrogenase assays. Cell injuries were characterized by morphological changes using hematoxylin and eosin staining. Reactive oxygen species, malondialdehyde and glutathione were measured to evaluate the levels of oxidative stress. To elucidate mechanisms, cell cycle distributions and the expressions of p53, p21 and Bax were also analyzed. Results showed that silica nanoparticles produced cytotoxicities in size, dose (0.1-1.6mg/ml) and time (12, 24, 36 and 48h exposure) dependent manners. Moreover, the particles caused oxidative stress, induced G1 phase arrest and upregulated levels of p53 and p21. Taken together, these data suggested that cell injuries were triggered by the generation of oxidative stress; p53 and p21 mediated G1 phase arrest is a potential mechanistic pathway of silica nanoparticles induced damage in H9c2(2-1) cells.