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Cytotoxic effect of zinc oxide nanoparticles on murine photoreceptor cells via potassium channel block and Na + /K + ‐ ATP ase inhibition
Author(s) -
Chen Chao,
Bu Wenjuan,
Ding Hongyan,
Li Qin,
Wang Dabo,
Bi Hongsheng,
Guo Dadong
Publication year - 2017
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12339
Subject(s) - cytotoxic t cell , potassium channel , cytotoxicity , biophysics , chemistry , potassium , lactate dehydrogenase , oxidative stress , reactive oxygen species , nanoparticle , membrane potential , inward rectifier potassium ion channel , zinc , potassium channel blocker , biochemistry , biology , enzyme , nanotechnology , ion channel , materials science , in vitro , receptor , organic chemistry
Objective Zinc oxide (ZnO) nanoparticles can exhibit toxicity towards organisms and oxidative stress is often hypothesized to be one of the most important factors. Nevertheless, the detailed mechanism of toxicity‐induced by ZnO nanoparticles has not been completely addressed. The present study aimed to investigate the toxic effects of ZnO nanoparticles on the expression and activity of Na + /K + ‐ ATP ase and on potassium channel block. Materials and methods In the present study, we explored the cytotoxic effect of ZnO nanoparticles on murine photoreceptor cells using lactate dehydrogenase ( LDH ) release assay, reactive oxygen species ( ROS ) determination, mitochondrial membrane potential (Δφm) measurement, delayed rectifier potassium current recordings and Na + /K + ‐ ATP ase expression and activity monitoring. Results The results indicated that ZnO nanoparticles could increase the LDH release in medium, aggravate the ROS level within cells, collapse the Δφm, block the delayed rectifier potassium current, and attenuate the expressions of Na + /K + ‐ ATP ase at both mRNA and protein levels and its activity, and thus exert cytotoxic effects on murine photoreceptor cells, finally damaging target cells. Conclusion Our findings will facilitate the understanding of the mechanism involved in ZnO nanoparticle‐induced cytotoxicity in murine photoreceptor cells via potassium channel block and Na + /K + ‐ ATP ase inhibition.

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