Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5848676 | Environmental Toxicology and Pharmacology | 2016 | 21 Pages |
Abstract
In probing the underlying mechanisms of nickel(II)-induced cytotoxicity on nasal epithelium, we investigated the effects of nickel(II) acetate on nasal epithelial RPMI-2650 cells. Nickel(II) elicited apoptosis, as signified by pyknotic and fragmented nuclei, increased caspase-3/7 activity, and an increase in annexin V binding, hypodiploid DNA, and Bax/Bcl-2 protein ratio. Nickel(II)-induced G2/M arrest was associated with up-regulation of p21WAF1/CIP1 expression, decrease in phosphorylation at Thr161 of Cdc2, and down-regulation of cyclin B1. Associated with these responses, ROS generation and mitochondrial depolarization increased in a nickel(II) concentration-dependent fashion. Pretreatment with N-acetylcysteine (NAC) attenuated these changes. p53 reporter gene assay and analyses of p53, Puma, Bax, and Bcl-2 protein levels indicated that NAC inhibited nickel(II)-induced activation of p53-mediated mitochondrial apoptotic pathway. Collectively, our study provides evidences that nickel(II) may induce oxidative damage on nasal epithelium in which antioxidant NAC protects cells against nickel(II)-induced apoptosis through the prevention of oxidative stress-mediated mitochondrial damage.
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Authors
Yoon-Jin Lee, Soo-Sung Lim, Byoung Joon Baek, Je-Min An, Hae-Seon Nam, Kee-Min Woo, Moon-Kyun Cho, Sung-Ho Kim, Sang-Han Lee,