New materials of emerging technological importance are single-walled carbon nanotubes (SWCNTs). Because SWCNTs will be used in commercial products in huge amounts, their effects on human health and the environment have been addressed in several studies. Inhalation studies in vivo and submerse applications in vitro have been described with diverging results. Why some indicate a strong cytotoxicity and some do not is what we report on here. Data from A549 cells incubated with carbon nanotubes fake a strong cytotoxic effect within the MTT assay after 24 h that reaches roughly 50%, whereas the same treatment with SWCNTs, but detection with WST-1, reveals no cytotoxicity. LDH, FACSassisted mitochondrial membrane potential determination, and Annexin-V/PI staining also reveal no cytotocicity. SWCNTs appear to interact with some tetrazolium salts such as MTT but not with others (such as WST-1, INT, XTT). This interference does not seem to affect the enzymatic reaction but lies rather in the insoluble nature of MTT−formazan. Our findings strongly suggest verifying cytotoxicity data with at least two or more independent test systems for this new class of materials (nanomaterials). Moreover, we intensely recommend standardizing nanotoxicological assays with regard to the material used: there is a clear need for reference materials. MTT−formazan crystals formed in the MTT reaction are lumped with nanotubes and offer a potential mechanism to guide bioremediation and clearance for SWCNTs from "contaminated" tissue. SWCNTs are good supporting materials for tissue growth, as attachment of focal adhesions and connections to the cytoskeleton suggest.

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BackgroundPulmonary surfactant reduces surface tension and is present at the air-liquid interface in the alveoli where inhaled nanoparticles preferentially deposit. We investigated the effect of titanium dioxide (TiO2) nanosized particles (NSP) and microsized particles (MSP) on biophysical surfactant function after direct particle contact and after surface area cycling in vitro. In addition, TiO2 effects on surfactant ultrastructure were visualized.MethodsA natural porcine surfactant preparation was incubated with increasing concentrations (50-500 μg/ml) of TiO2 NSP or MSP, respectively. Biophysical surfactant function was measured in a pulsating bubble surfactometer before and after surface area cycling. Furthermore, surfactant ultrastructure was evaluated with a transmission electron microscope.ResultsTiO2 NSP, but not MSP, induced a surfactant dysfunction. For TiO2 NSP, adsorption surface tension (γads) increased in a dose-dependent manner from 28.2 ± 2.3 mN/m to 33.2 ± 2.3 mN/m (p < 0.01), and surface tension at minimum bubble size (γmin) slightly increased from 4.8 ± 0.5 mN/m up to 8.4 ± 1.3 mN/m (p < 0.01) at high TiO2 NSP concentrations. Presence of NSP during surface area cycling caused large and significant increases in both γads (63.6 ± 0.4 mN/m) and γmin (21.1 ± 0.4 mN/m). Interestingly, TiO2 NSP induced aberrations in the surfactant ultrastructure. Lamellar body like structures were deformed and decreased in size. In addition, unilamellar vesicles were formed. Particle aggregates were found between single lamellae.ConclusionTiO2 nanosized particles can alter the structure and function of pulmonary surfactant. Particle size and surface area respectively play a critical role for the biophysical surfactant response in the lung.

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BackgroundPulmonary surfactant reduces surface tension and resembles the air−liquid interface in the alveoli where inhaled nanoparticles preferentially deposit. We investigated the effect of titanium dioxide (TiO2) nanoparticles (NP) and microparticles (MP) on biophysical surfactant function after direct particle contact and after surface area cycling in vitro. In addition, TiO2 NP effects on surfactant ultrastructure were visualized. Methods A porcine surfactant preparation (1.5 mg/ml) was incubated with increasing concentrations (0−500 µg/ml) of TiO2 NP or MP. Biophysical surfactant function was measured in a pulsating bubble surfactometer before and after surface area cycling, which was done at 37°C for 8 hours (0.43 Hz). Furthermore, surfactant ultrastructure was evaluated with a transmission electron microscope. ResultsTiO2 NP but not MP induced a slight surfactant dysfunction. Adsorption surface tension (γads) dose dependently increased from 27.9 ± 4.4 mN/m to 32.5 ± 8.3 mN/m. Surface tension at minimum bubble size only slightly increased from 4.9 ± 1.9 mN/m up to 8.1 ± 4.5 mN/m at high TiO2 concentrations. Presence of NP during surface area cycling markedly increased γads up to 63.6 ± 1.0 mN/m. Surface tension at minimum bubble size increased dramatically to 21.1 ± 0.7 mN/m. Interestingly, TiO2 NP induced aberrations in the surfactant ultrastructure. Lamellar body like structures were decreased in size and deformed. Unilamellar vesicles were induced. In addition, TiO2 particle aggregates were found between single lamellae. Conclusion TiO2 nanoparticles can alter the structure and function of pulmonary surfactant. This abstract is funded by: DFG SFB 587/B8 and Fraunhofer ITEM. Am J Respir Crit Care Med 179;2009:A5255 Internet address: www.atsjournals.org Online Abstracts Issue

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