| BackgroundThe notable growth of mobile telecommunications utilization has aroused public concerns for possible adverse effects induced by radiofrequency fields (RF). Oxidative stress, defined as an imbalance between oxidants and antioxidants in favor of the former, is an important factor contributing to several biochemical changes and human chronic conditions. Although studies of oxidative stress associated with RF exposure in vivo or in vitro have been conducted, these investigations have yielded inconsistent results, and the mechanism of RF induction of oxidative stress is still not clear. Many ophthalmological disorders are associated with oxidative stress, as well as biological effects of RF radiation on lens epithelial cells (LECs) have been reported. Thus, it is necessary to determine whether exposure to low-intensity RF can result in oxidative stress in LECs and to explore possible causes of RF-induced effects at the molecular biological level.ObjectiveThe aims of the present study were to determine oxidative stress and to explore possible reasons of reactive oxygen species (ROS) increase in human lens epithelial (HLE) B3cells exposed to low intensity1.8GHz RF.MethodsThe HLE B3cells were divided into RF exposure and RF sham-exposure groups. The RF exposure intensity was at specific absorption rate (SAR) of2,3, or4W/kg. The ROS levels were measured by a fluorescent probe2’7’-dichlorofluorescin diacetate (DCFH-DA) assay in the HLE B3cells exposed to1.8GHz RF for0.5,1, and1.5h. Lipid peroxidation and cellular viability were detected by an malondialdehyde (MDA) test and Cell Counting Kit-8(CCK-8) assay in the HLE B3cells exposed to1.8GHz RF for6,12, and24h, respectively. The mRNA expression of SOD1, SOD2, CAT, and GPxl genes and the expression of SOD1, SOD2, CAT, and GPx1proteins were measured by qRT-PCR and Western blot assays in the HLE B3cells exposed to1.8GHz RF for1h.ResultsThe ROS and MDA levels significantly increased (P<0.05) in the RF exposure group and the cellular viability, mRNA expression of four genes, and expression of four proteins significantly decreased (P<0.05) compared with the RF sham-exposure group.ConclusionOxidative stress is present in HLE B3cells exposed to1.8GHz low-intensity RF and the increased production of ROS may be related to down-regulation of four antioxidant enzyme genes induced by RF exposure. |