Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Abstract

The inhalation of engineered nanoparticles stimulates the development of atherosclerosis and impairs vascular function. However, the cardiac effects of inhaled engineered nanoparticles are unknown. Here, we investigate the effects of ultrafine titanium dioxide (UFTiO₂) on the heart, and we define the possible mechanisms underlying the measured effects. Pulmonary exposure of rats to UFTiO₂ increased the phosphorylation levels of p38 mitogen-activated protein kinase and cardiac troponin I, but not Akt, in the heart and substance P synthesis in nodose ganglia. Circulatory levels of pro-inflammatory cytokines, and blood cell counts and differentials were not significantly changed after pulmonary exposure. Separately, the incubation of cardiac myocytes isolated from naïve adult rat hearts in vitro with UFTiO₂ did not alter the phosphorylation status of the same cardiac proteins. In conclusion, the inhalation of UFTiO₂ enhanced the phosphorylation levels of cardiac proteins. Such responses are likely independent of systemic inflammation, but may involve a lung-neuron-regulated pathway.

Keywords::

• Nanoparticles
• cardiovascular diseases
• titanium dioxide
• inhalation study

Acknowledgement

The authors would like to thank Rebecca Salmen for her excellent technical support.

Notes