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|Title:||Characterisation of cadmium chloride induced molecular and functional alterations in bronchial epithelial cells|
|Authors:||FORTI Efrat; BULGHERONI A.; CETIN Yuksel; HARTUNG Thomas; JENNINGS Paul; PFALLER Walter; PRIETO PERAITA Maria Del Pilar|
|Citation:||CELLULAR PHYSIOLOGY AND BIOCHEMISTRY vol. 25 p. 159-168|
|Type:||Articles in Journals|
|Abstract:||Epidemiological studies show that cadmium (Cd) exposure causes pulmonary damage, such as emphysema, pneumonitis and lung cancer. However, the mechanisms leading to pulmonary toxicity are not yet fully elucidated. The aim of this study was to further investigate CdCl2 induced toxicity using Calu-3 cells as an in vitro model of human bronchial epithelial cells. CdCl2 induced effects following either apical or basolateral exposure were evaluated by Neutral Red Uptake (NRU), Trans-Epithelial Electrical Resistance (TEER), and alteration in Metallothionein 1X (MT1X), Heat shock 70 (HSP70), and Heme oxygenase 1 (HMOX-1) genes. CdCl2 exposure resulted in a collapse of barrier function and the induction of MT1X, HMOX-1 and HSP70, prior to alterations in cell viability. These effects were more potent when exposure was basolateral. Co-administration of N-Acetylcysteine (NAC) exerted a strong protective effect on CdCl2 induced barrier damage and stress related genes, while other antioxidants only attenuated Cd induced HSP70 and HMOX-1 and showed no protective effect on the barrier collapse. These findings indicate that Cd exposure is likely to impair Calu-3 barrier function at non cytotoxic concentrations by direct effect on adherens junction proteins. The protective effect of NAC against Cd induced MT1X, HSP70 and HMOX-1 genes demonstrates an anti-oxidant effect of NAC in addition to Cd chelation.|
|JRC Institute:||Institute for Health and Consumer Protection|
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