Oxygen Metabolism in the Cardiorespiratory System after an Acute Exposure to Ni-doped Nanoparticles

MAGNANI, NATALIA; GARCÉS, MARIANA; MARCHINI, TIMOTEO; CACERES, LOURDES; GUAGLIANONE, ALEJANDRO; MEBERT, ANDREA; DIAZ, LUIS; DESIMONE, MARTIN; ALVAREZ, SILVIA; EVELSON, PABLO

Chicago, Illinois

Simposio; Society of Free Radical Biology and Medicine Redox Symposium; 2016

Society of Free Radical Biology and Medicine

There is strong evidence that ambient air pollution particles present a serious risk to human health. Numerous epidemiological studies have shown an association between airborne particulate matter (PM) and increased cardiopulmonary morbidity and mortality. Transition metals, such as nickel, are frequent PM constituents and might play a central role in cardiopulmonary disease mechanisms initiated by PM exposure. The aim of this work was to analyze the cardiorespiratory oxidative metabolism after an acute exposure to Ni-doped silica nanoparticles (Ni-NP). Swiss mice (20-25 g) were intranasally instilled with a Ni-NP suspension (1.0 mg Ni/kg body weight), delivered in a single dose. The control group was exposed to a silica NP without Ni. Lung, heart, and blood samples were collected 1 h after the exposure. NP share comparable physicochemical properties with air pollution PM in size (Control: 170 ± 2 nm; Ni-NP: 200 ± 20 nm) and shape, as observed by TEM. Lungs from Ni-NP-exposed mice showed increased tissue O2 consumption (67%; p˂0.001), NADPH oxidase (Nox) activity (41%; p˂0.001) and TBARS content (35%; p˂0.001) compared to control group, while GSH/GSSG ratio was decreased in the treated group (p˂0.05). TBARS content in plasma was found increased by 54% (p˂0.001) in Ni-NP group. In heart samples, O2 consumption rates were decreased in Ni-NP mice (37%; p˂0.0001). The use of metal coated NP was a useful approach to evaluate the effect of the metal ions present in air particles, since they are exposed in a similar way than PM. Taken together, these results show that the exposure to Ni-NP induces impaired oxidative metabolism in lung and heart. These findings contribute to the understanding of the cardiopulmonary toxicity of PM exposure, where oxidative stress and inflammation may play a predominant role in association with transition metals present in environmental PM.