Carbon nanotubes show no sign of acute toxicity but induce intracellular reactive oxygen species in dependence on contaminants.

Today nanosciences are experiencing massive investment worldwide although research on toxicological aspects of these nano-sized particles has just begun and to date, no clear guidelines exist to quantify the effects. In the present study, we focus on carbon nanotubes (CNTs), which represent one of the most widely investigated carbon nanoparticles. The present data indicate that CNTs are able to cross the cell membrane of rat macrophages (NR8383) and, therefore, might have an influence on cell physiology and function. NR8383 and human A549 lung cells were incubated with commercial single-walled (NT-1) and multi-walled (NT-2, NT-3) CNTs, carbon black and quartz as reference particles as well as an acid-treated single-walled CNT preparation (SWCNT a.t.) with reduced metal catalyst content. We did not observe any acute toxicity on cell viability (WST-1, PI-staining) upon incubation with all CNT products. None of the CNTs induced the inflammatory mediators NO, TNF-alpha and IL-8. A rising tendency of TNF-alpha release from LPS-primed cells due to CNT treatment could be observed. We detected however, a dose- and time-dependent increase of intracellular reactive oxygen species and a decrease of the mitochondrial membrane potential with the commercial CNTs in both cell types after particle treatment whereas incubation with the purified CNTs (SWCNT a.t.) had no effect. This leads us to the conclusion that metal traces associated with the commercial nanotubes are responsible for the biological effects.