Abstract

Liquid crystal displays (LCDs) are used as screens in consumer electronics and are indispensable in the modern era of computing. LCDs utilize light-emitting diodes (LEDs) as backlight modules and emit high levels of blue light, which may cause retinal photoreceptor cell damage. However, traditional blue light filters may decrease the luminance of light and reduce visual quality. We adjusted the emitted light spectrum of LED backlight modules in LCDs and reduced the energy emission but maintained the luminance. The 661W photoreceptor cell line was used as the model system. We established a formula of the ocular energy exposure index (OEEI), which could be used as the indicator of LCD energy emission. Cell viability decreased and apoptosis increased significantly after exposure to LCDs with higher emitted energy. Cell damage occurred through the induction of oxidative stress and mitochondrial dysfunction. The molecular mechanisms included activation of the NF-κB pathway and upregulation of the expression of proteins associated with inflammation and apoptosis. The effect was correlated with OEEI intensity. We demonstrated that LCD exposure-induced photoreceptor damage was correlated with LCD energy emission. LCDs with lower energy emission may, therefore, serve as suitable screens to prevent light-induced retinal damage and protect consumers’ eye health.

Highlights

  • Computers and consumer electronics play important roles in modern society; the majority of these products use a liquid crystal display (LCD) as the screen with light-emitting diode (LED)-based backlight modules being widely used as the Liquid crystal displays (LCDs) light source

  • In order to determine the appropriate conditions for light-induced retinal photoreceptor cell damage, we investigated the viability of 661W with different duration (1, 2, and 3 days) and luminance (100, 200, and 300 nits) of LCD exposure

  • The results of the present study indicated that LCDs with higher ocular energy exposure index (OEEI) caused stronger light-induced photoreceptor cell damage through the production of reactive oxygen species (ROS) and activation of the NF-κB pathway, along with upregulation of protein expression associated with inflammatory response and apoptosis

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Summary

Introduction

Computers and consumer electronics play important roles in modern society; the majority of these products use a liquid crystal display (LCD) as the screen with light-emitting diode (LED)-based backlight modules being widely used as the LCD light source. LEDs emit higher levels of blue light with shorter wavelengths than conventional light sources and are accompanied by an enhanced risk of photo-injury. Extensive blue light exposure disrupts circadian rhythms [1], which may constitute a health hazard for humans. LED-induced retinal photoreceptor and RPE cell damage have been observed in several animal studies [9,10], even at domestic lighting levels [11]. Previous studies found that the mechanism of retinal injury is related to the generation of reactive oxygen species (ROS) and inflammatory reactions, which induce oxidative stress and cell apoptosis within the retina [15,16,17,18,19]

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