Abstract:
:Zinc is an essential element for the biological system. However, excessive exogenous Zn2+ would disrupt cellular Zn2+ homeostasis and cause toxicity. In particular, Zinc salts or ZnO nanoparticles exposure could induce respiratory injury. Although previous studies have indicated that organelle damage (including mitochondria or lysosomes) and reactive oxygen species (ROS) production are involved in Zn2+-induced toxicity, the interplay between mitochondria/lysosomes damage and ROS production is obscure. Herein, we demonstrated that Zn2+ could induce deglycosylation of lysosome-associated membrane protein 1 and 2 (LAMP-1 and LAMP-2), which primarily locate in late endosomes/lysosomes, in A549 lung epithelium cells. Intriguingly, LAMP-2 knockdown further aggravated Zn2+-mediated ROS production and cell death, indicating LAMP-2 (not LAMP-1) was involved in Zn2+-induced toxicity. Our results provide a new insight that LAMP-2 contributes to the ROS clearance and cell death induced by Zn2+ treatment, which would help us to get a better understanding of Zn2+-induced toxicity in respiratory system.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Qin X,Zhang J,Wang B,Xu G,Zou Zdoi
10.1016/j.bbrc.2017.05.030subject
Has Abstractpub_date
2017-06-17 00:00:00pages
177-181issue
1eissn
0006-291Xissn
1090-2104pii
S0006-291X(17)30889-6journal_volume
488pub_type
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