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Preferential killing of cancer cells and activated human T cells using ZnO nanoparticles

Cory Hanley et al 2008 Nanotechnology 19 295103 (10pp)   doi: 10.1088/0957-4484/19/29/295103  Help

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Cory Hanley1, Janet Layne1, Alex Punnoose2, K M Reddy2, Isaac Coombs2, Andrew Coombs2, Kevin Feris1 and Denise Wingett1,3,4,5
1 Department of Biological Sciences, Boise State University, Boise, ID 83725, USA
2 Department of Physics, Boise State University, Boise, ID 83725, USA
3 Department of Medicine, Division of Gerontology and Geriatric Medicine, University of Washington, Seattle, WA 98195, USA
4 MSTMRI Research Institute of St Luke's Regional Medical Center, Boise, ID 83712, USA
5 Address for correspondence: Department of Biological Sciences, Boise State University, 1910 University Drive, Boise, ID 83725, USA
E-mail: denisewingett@boisestate.edu

Abstract. Nanoparticles are increasingly being recognized for their potential utility in biological applications including nanomedicine. Here we examine the response of normal human cells to ZnO nanoparticles under different signaling environments and compare it to the response of cancerous cells. ZnO nanoparticles exhibit a strong preferential ability to kill cancerous T cells (~28–35 ×) compared to normal cells. Interestingly, the activation state of the cell contributes toward nanoparticle toxicity, as resting T cells display a relative resistance while cells stimulated through the T cell receptor and CD28 costimulatory pathway show greater toxicity in direct relation to the level of activation. Mechanisms of toxicity appear to involve the generation of reactive oxygen species, with cancerous T cells producing higher inducible levels than normal T cells. In addition, nanoparticles were found to induce apoptosis and the inhibition of reactive oxygen species was found to be protective against nanoparticle induced cell death. The novel findings of cell selective toxicity, towards potential disease causing cells, indicate a potential utility of ZnO nanoparticles in the treatment of cancer and/or autoimmunity.

Print publication: Issue 29 (23 July 2008)
Received 15 February 2008
Published 10 June 2008

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