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Nickel nanoparticles contribute to cancer in human lung cells, in vitro study suggests
Created by assoceditor on 25/08/2011 12:08:53

New research by an interdisciplinary team of scientists at Brown University has found that nickel nanoparticles activate a cellular pathway that contributes to cancer in human lung cells.


In a study published this month in the journal Toxicological Sciences, researchers from Brown University, USA, have published results of an in vitro study which indicates that nickel nanoparticles have the potential to active a cellular pathway that contributes to cancer in human lung cells.

"Nanotechnology has tremendous potential and promise for many applications," said Agnes Kane, Chair of the Department of Pathology and Laboratory Medicine in The Warren Alpert Medical School of Brown University ans senior author of the study. "But the lesson is that we have to learn to be able to design them more intelligently and, if we recognise the potential hazards, to take adequate precautions."

Nickel nanoparticles have already been shown to be harmful, but not in terms of cancer. Kane and co-workers found evidence that ions on the surface of the particles are released inside human epithelial lung cells to jumpstart a pathway called HIF-1 alpha. Normally the pathway helps trigger genes that support a cell in times of low oxygen supply, a problem called hypoxia, but it is also known to encourage tumour cell growth.

"Nickel exploits this pathway, in that it tricks the cell into thinking there’s hypoxia but it’s really a nickel ion that activates this pathway," said Kane, whose work is supported by a National Institutes of Health Superfund Research Program Grant. "By activating this pathway it may give premalignant tumour cells a head start."

The research team, led by postdoctoral research associate and first author Jodie Pietruska, exposed human lung cells to nanoscale particles of metallic nickel and nickel oxide, and larger microscale particles of metallic nickel. A key finding from the study is that while nano-scale nickel particles set off the HIF-1 alpha pathway, larger microscale metallic nickel particles proved much less problematic.  According to Kane, the reason for this might be that, for the same amount of metal by mass, nanoscale particles expose much more surface area and are thus much more chemically reactive than microscale particles.

Another important result from the work is data showing a big difference in how nickel nanoparticles and nickel oxide nanoparticles react with cells, Pietruska said. The nickel oxide particles are so lethal that the cells exposed to them died quickly, leaving no opportunity for cancer to develop. Metallic nickel particles, on the other hand, were less likely to kill the cells. That could allow the hypoxia pathway to lead to the cell becoming cancerous.

"What is concerning is the metallic nickel nanoparticles caused sustained activation but they were less cytotoxic," Pietruska said. "Obviously a dead cell can’t be transformed."

Although Kane said the findings should raise clear concerns about handling nickel nanoparticles, for instance to prevent airborne exposure to them in manufacturing, they are not all that’s needed to cause cancer. Cancer typically depends on a number of unfortunate changes, Kane clarified. It is also important to highlight that this study looked at the short-term effects of nickel nanoparticle exposure in cells in a lab, rather than over the long term in a whole organism.

Reference: J. R. Pietruska, X. Liu, A. Smith, K. McNeil, P. Weston, A. Zhitkovich, R. Hurt, A. B. Kane. Bioavailability, intracellular mobilization of nickel, and HIF-1α activation in human lung epithelial cells exposed to metallic nickel and nickel oxide nanoparticles.Toxicological Sciences, 2011.

Source: Brown University Press Release

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