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Journal of Immunology Research
Volume 2014 (2014), Article ID 295092, 8 pages
Research Article

Palladium Nanoparticles Induce Disturbances in Cell Cycle Entry and Progression of Peripheral Blood Mononuclear Cells: Paramount Role of Ions

1Immunotoxicology and Allergy Unit, Ce.S.I., “G. d’Annunzio” University Foundation, 66100 Chieti, Italy
2Department of Medicine and Ageing Science, “G. d’Annunzio” University, 66100 Chieti, Italy
3Unit of General Pathology, Ce.S.I., “G. d’Annunzio” University Foundation and Department of Medicine, Dentistry and Biotechnology, G. d’Annunzio University, 66100 Chieti, Italy
4University of Ulm, Institute for Analytical and Bioanalytical Chemistry, 89081 Ulm, Germany
5Laboratorio di Biopatologia Ultrastrutturale, Department of Experimental Medicine, University of Rome “La Sapienza”, 00161 Rome, Italy
6Shanxi Medical University, Taiyuan, China
7Department of Biotechnology and Molecular Sciences, University of Insubria, 21100 Varese, Italy
8The Protein Factory, Interuniversity Centre Politecnico di Milano, ICRM CNR Milano and University of Insubria, 20131 Milan, Italy

Received 5 March 2014; Revised 6 June 2014; Accepted 8 June 2014; Published 3 July 2014

Academic Editor: Andrij Holian

Copyright © 2014 Claudia Petrarca et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


There is concern about the possible toxicity of palladium nanoparticles (Pd-NP), as they are released in the environment through many applications. We previously studied the toxicity of Pd-NP at high concentrations; here we address the possible toxicity of Pd-NP at low, subtoxic doses. In particular, we have exposed normal human PBMC entering into the first in vitro mitotic division to Pd-NP and to Pd(IV) ions to evaluate ROS generation and cell cycle progression. We have measured a statistically significant increase of intracellular ROS in Pd(IV) exposed cells, but not in Pd-NP exposed cells. TEM revealed accumulation of lipid droplets and autophagic and mitophagic vacuoles, which appeared more conspicuous in cells exposed to Pd(IV) ions than to Pd-NP. Pd-NP were visible in the cytoplasm of Pd-NP exposed cells. Pd-NP addition was associated with a significant increase of cells within the G0/G1-phase and a significant reduction in GS- and G2/M-phases. Cells exposed to Pd(IV) ions showed a significant amplification of these cell cycle alterations. These results suggest that ions, per se or released by NPs, are the true inducers of Pd toxicity. It will be essential to verify whether the observed disturbance represents a temporary response or might result in permanent alterations.