Pulmonary Cerium Dioxide Nanoparticles Exposure Differentially Impairs Coronary and Mesenteric Arteriolar Reactivity

Cerium dioxide nanoparticles (CeO 2 NPs) are an engineered nanomaterial that possesses unique catalytic, oxidative and reductive properties. Currently, CeO 2 NPs are being used as a fuel catalyst but these properties are also utilized in the development of potential drug treatments for radiation and...

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Bibliographic Details
Published inCardiovascular toxicology Vol. 13; no. 4
Main Authors Minarchick, Valerie C, Stapleton, Phoebe A, Porter, Dale W, Wolfarth, Michael G, Çiftyürek, Engin, Barger, Mark, Sabolsky, Edward M., Nurkiewicz, Timothy R
Format Journal Article
LanguageEnglish
Published 01.12.2013
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Summary:Cerium dioxide nanoparticles (CeO 2 NPs) are an engineered nanomaterial that possesses unique catalytic, oxidative and reductive properties. Currently, CeO 2 NPs are being used as a fuel catalyst but these properties are also utilized in the development of potential drug treatments for radiation and stroke protection. These uses of CeO 2 NPs present a risk for human exposure; however, to date no studies have investigated the effects of CeO 2 NPs on the microcirculation following pulmonary exposure. Previous studies in our laboratory with other nanomaterials have shown impairments in normal microvascular function after pulmonary exposures. Therefore, we predicted that CeO 2 NP exposure would cause microvascular dysfunction that is dependent on the tissue bed and dose. Twenty-four hour post exposure to CeO 2 NPs (0–400 μg), mesenteric and coronary arterioles were isolated and microvascular function was assessed. Our results provided evidence that pulmonary CeO 2 NP exposure impairs endothelium-dependent and -independent arteriolar dilation in a dose-dependent manner. The CeO 2 NP exposure dose which causes a 50% impairment in arteriolar function (EC 50 ) was calculated and ranged from 15 – 100 μg depending on the chemical agonist and microvascular bed. Microvascular assessments with acetylcholine revealed a 33–75% reduction in function following exposure. Additionally, there was a greater sensitivity to CeO 2 NP exposure in the mesenteric microvasculature due to the 40% decrease in the calculated EC 50 compared to the coronary microvasculature EC 50 . CeO 2 NP exposure increased mean arterial pressure in some groups. Taken together these observed microvascular changes may likely have detrimental effects on local blood flow regulation and contribute to cardiovascular dysfunction associated with particle exposure.
ISSN:1530-7905
1559-0259
DOI:10.1007/s12012-013-9213-3