Nickel(II)-induced nasal epithelial toxicity and oxidative mitochondrial damage
- 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 p21(WAF1/CIP1) expression, decrease in phosphorylation at Thr(161) 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.
- All Author(s)
- Y. J. Lee
; S. S. Lim
; B. J. Baek
; J. M. An
; H. S. Nam
; K. M. Woo
; M. K. Cho
; S. H. Kim
; S. H. Lee
- Issued Date
- 2016
- Type
- Article
- Keyword
- Nickel(II) acetate; Nasal epithelium; G2/M arrest; Apoptosis; Oxidative damage; N-acetylcysteine
- ISSN
- 1382-6689
- Citation Title
- Environmental Toxicology and Pharmacology
- Citation Volume
- 42
- Citation Start Page
- 76
- Citation End Page
- 84
- Language(ISO)
- eng
- DOI
- 10.1016/j.etap.2016.01.005
- URI
- http://schca-ir.schmc.ac.kr/handle/2022.oak/2619
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