Modifications of carbon black nanoparticle surfaces modulate type II pneumocyte homoeostasis.

Inhalation uptake of carbon black nanoparticles (CBNP) bears the risk of morphological and functional lung impairment attributed to the highly reactive particle surface area. Chemical particle surface modifications might affect particle-cell interactions; however, thus far these alterations have not been determined. This is the first in vivo study comparing particle-induced acute lung injury using Printex(®)90 (Pr90, 7 µg), Printex®90 covered by benzo[a]pyrene or 9-nitroanthracene (BaP-Pr90, NA-Pr90, 7 µg, 15% BaP or NA by weight), and acetylene carbon black (CB) with polycyclic aromatic hydrocarbons (PAH-AB, 7 µg, 20% PAH by weight).

Nitration of protein without allergenic potential triggers modulation of antioxidant response in type II pneumocytes.

Inhalation of nitrogen and reactive oxygen species (ROS) is known to induce lung inflammation, which is prevented by enzymatic and nonenzymatic antioxidant systems. These agents form nitrated allergens that were shown to enhance allergenicity. The aim of this study was to examine the influence of nitrated proteins on inflammation and antioxidant status of the lung.

Lung alterations following single or multiple low-dose carbon black nanoparticle aspirations in mice.

Carbon black nanoparticle (CBNP) applications in high doses have been shown to be harmful to the lung. It is postulated that even small, environmentally relevant concentrations induce changes on lung homeostasis. The present study determined the impact of low-dose single and multiple CBNP (Printex 90) applications on mouse alveolar cell metabolism, especially inflammatory and oxidative stress parameters.

NO2-induced acute and chronic lung injury cause imbalance of glutathione metabolism in type II pneumocytes.

Background: During inspiration the lung is exposed to numerous oxidants and therefore has developed a system of antioxidant defense. This organ, besides the liver, is the major source of glutathione (GSH) metabolism, from which type II pneumocytes are metabolically the most active cells.

Material/methods: To analyze oxidative stress, rats were exposed to air (control) or to 10 ppm nitrogen dioxide (NO2) for 3 and 20 days to induce acute and chronic lung injury.