Silica nanoparticles induce cardiomyocyte apoptosis via the mitochondrial pathway in rats following intratracheal instillation

Diseases of the cardiac system caused by silicon dioxide exposure have captured wide public attention. Upon entering the blood circulation, ultrafine particles have the potential to influence cardiomyocytes, leading to myocardial ischemia or even cardiac failure, and the molecular mechanisms remain to be completely elucidated. In this study, the toxicity of ultrafine particles on cardiomyocytes from rats exposed to silica nanoparticles was observed. Rats were randomly divided into a normal saline control group and three exposure groups (2, 5 and 10 mg/kg<bold>body weight</bold>) that were intratracheally treated with 60-nm silica nanoparticles. Alterations in body weight, routine blood factors and myocardial enzymes, histopathological and microstructural alterations, apoptosis and the expression of apoptosis-associated proteins were assessed at the end of the exposure period. The silicon levels in the heart and serum, and myocardial enzymes in exposed rats were significantly increased in a dose-dependent manner. In addition, exposure to the silica nanoparticles caused notable histological and ultrastructural alterations in the hearts of these animals. Furthermore, a significant apoptotic effect was observed in the exposure groups. The present data suggest that silica nanoparticles may enter the circulatory system through the lungs, and are distributed to the heart causing cardiovascular injury. Silica nanoparticle-induced apoptosis via the mitochondrial pathway may serve an important role in observed cardiac damage.