Premium
UVB Irradiation Enhances TiO 2 Nanoparticle‐induced Disruption of Calcium Homeostasis in Human Lens Epithelial Cells
Author(s) -
Wu Qiuxin,
Guo Dadong,
Du Yuxiang,
Liu Dongmei,
Wang Daoguang,
Bi Hongsheng
Publication year - 2014
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/php.12322
Subject(s) - intracellular , calcium in biology , reactive oxygen species , calcium , microbiology and biotechnology , chemistry , homeostasis , cell growth , calcium metabolism , downregulation and upregulation , cell , plasma membrane ca2+ atpase , biophysics , atpase , biology , biochemistry , enzyme , organic chemistry , gene
Currently, titanium dioxide nanoparticles (TiO 2 NP s) have been widely used in various applications including cosmetics, food additives and biomedicine. However, there are few reports available using TiO 2 NP s to treat ocular diseases. Posterior capsular opacification ( PCO ) is the most frequent complication after cataract surgery, which is induced by the proliferation and migration of lens epithelial cells. Thus, inhibiting the proliferation of lens epithelial cells will efficiently reduce the occurrence of PCO . In this study, we investigated the effects of TiO 2 NP s on HLE B‐3 cells with or without ultraviolet B ( UVB ) irradiation in vitro . We found that TiO 2 NP s can inhibit HLE B‐3 cell growth, cause the elevation of intracellular [Ca 2+ ], produce excessive reactive oxygen species ( ROS ), further reduce Ca 2+ ‐ ATP ase activity and decrease the expression of plasma membrane calcium ATP ase 1 ( PMCA 1), finally disrupt the intracellular calcium homeostasis and induce cell damage. Importantly, UVB irradiation can apparently enhance these effects on HLE B‐3 cells in the presence of TiO 2 NP s. Taken together, the generation of excessive ROS and the disruption of intracellular calcium homeostasis may be both involved in TiO 2 nanoparticle‐induced HLE B‐3 cell damage under UVB irradiation.