Chao Chen1,2, Wenjuan Bu2, Hongyan Ding3, Qin Li4, Dabo Wang1, Hongsheng Bi5, Dadong Guo5. 1. Department of Ophthalmology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China. 2. Department of Ophthalmology, The First People's Hospital of Jining, Jining, Shandong Province, China. 3. Jiangsu Provincial Key Laboratory for Interventional Medical Devices, Huaiyin Institute of Technology, Huaian, Jiangsu Province, China. 4. Department of Integration of Chinese and Western Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong Province, China. 5. Eye Institute of Shandong University of Traditional Chinese Medicine, Jinan, Shandong Province, China.
Abstract
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.
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.
Authors: Filip Sawosz; Lane Pineda; Anna Hotowy; Sławomir Jaworski; Marta Prasek; Ewa Sawosz; André Chwalibog Journal: Arch Anim Nutr Date: 2013-08-16 Impact factor: 2.242