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+ -ATPase 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+ -ATPase 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+ -ATPase 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+ -ATPase inhibition.
Keywords: Na+/K+-ATPase; delayed rectifier potassium current; murine photoreceptor cell; reactive oxygen species; zinc oxide nanoparticle.
© 2017 John Wiley & Sons Ltd.