Please use this identifier to cite or link to this item:
|Title:||In vitro evaluation of the toxicity induced by nickel soluble and particulate forms in human airway epithelial cells|
|Authors:||FORTI Efrat; SALOVARA Susan; CETIN Yuksel; BULGHERONI Anna; TESSADRI Richard; JENNINGS Paul; PFALLER Walter; PRIETO PERAITA Maria Del Pilar|
|Citation:||TOXICOLOGY IN VITRO vol. 25 no. 2 p. 454-461|
|Publisher:||PERGAMON-ELSEVIER SCIENCE LTD|
|Type:||Articles in Journals|
|Abstract:||Epidemiological studies show that exposure to nickel (Ni) compounds is associated with a variety of pulmonary adverse health effects such as lung inflammation, fibrosis, emphysema and tumours. However, the mechanisms leading to pulmonary toxicity are not yet fully elucidated. In the current study we used Calu-3, a well differentiated human bronchial cell line, to investigate in vitro the effect Ni in soluble form (NiCl2) and micro-sized Ni particles (Type 210) on the airway epithelium. For this purpose we evaluated the effect of Ni compounds on the epithelial barrier integrity by monitoring the transepithelial electrical resistance (TEER) and on oxidative stress pathways by measuring reactive oxygen species (ROS) formation and induction of stress-inducible genes. Our results showed that exposure to NiCl2 and Ni particles resulted in a disruption of the barrier function observed by alterations in TEER that occurred prior to the decrease in cell viability. Moreover, Ni compounds induced oxidative stress associated with ROS formation and up-regulation of the stress- inducible genes, Metallothionein 1X (MT1X), Heat shock protein 70 (HSP70), Heme oxygenase-1 (HMOX-1), and gamma-glutamylcysteine synthetase (¿GCS). Furthermore, we have demonstrated that the induced effects by Ni compounds can be partially attributed to the increase in Ni ions intracellular levels.|
|JRC Institute:||Institute for Health and Consumer Protection|
Files in This Item:
There are no files associated with this item.
Items in repository are protected by copyright, with all rights reserved, unless otherwise indicated.