Liquid Crystal Displays Associated with Light-Induced Photoreceptor Damage

by | Jul 29, 2019 | 2019, Eye Health

Written by Angeline A. De Leon, Staff Writer. Researchers demonstrated that emission of blue light energy from LCD screens was associated with damage to retinal photoreceptor cells of the eye; therefore, LCD screens that emit lower levels of blue light may be more appropriate for protecting consumers’ eye health by reducing light-induced retinal damage.

computer useIn the contemporary age of electronics and mobile devices, the use of liquid crystal display (LCD) screens is rampant. LCDs use light-emitting diode (LED)-based modules as their light source, which is associated with blue light emission and risk of photoreceptor damage 1,2. Animal studies indicate that even at indoor lighting levels, LED exposure is linked to damage of retinal pigment epithelial (RPE) cells (pigmented cells forming the outer blood-retina barrier) 3,4. Exposure to short-wavelength light, like the kind emitted from LCDs, is thought to play a role in the development of age-related macular degeneration 5, primarily through formation of reactive oxygen species (ROS) and induction of oxidative stress within the retina 6. In an effort to protect against light-induced retinal injury, the use of blue light filters and blocking lenses have become popular 7, however, this is primarily accomplished through reducing luminance of light, which subsequently reduces visual quality. As an alternative option, researchers have begun to explore ways to reduce emitted wavelengths of LEDs while maintaining visual quality of screens 8. A recent study 9 published in the International Journal of Molecular Sciences investigated the potential photoreceptor damage induced by exposure to LCDs with different ocular energy exposure index (OEEI) values, a formula established by investigators as an indicator of LCD energy emission.

A 661W cell line, constituting a mouse photoreceptor cell line, was cultured and exposed to LCDs with luminance of 0, 100, 200, and 300 nits for 3 days. Alterations in morphology were observed, and cell viability was estimated using an assay kit. Establishing a formula of OEEI as the total radiance of the LCD visible spectrum divided by total luminance of the LCD, investigators used 21-inch LCDs with low, medium, and OEEI values (3.35 x 10-3, 3.53 x 10-3, 3.55 x 10-3 W/lm), with luminance maintained at 300 nits. Terminal deoxynucleotidyl transferase-mediated dUTP-biotinide end labeling (TUNEL) was used to analyze cell apoptosis, and intracellular ROS was measured using an ROS assay. Mitochondrial membrane potential was measured using an assay kit and a fluorescence microscope, and Western blot analysis was performed to quantify relative expression of proteins. Finally, electrophoretic mobility shift assay (EMSA) was performed to study the DNA-binding activity of nuclear factor-κB (NF-κB, proinflammatory signaling pathway).

Cell viability was seen to significantly decrease after 3 days of exposure to LCDs with medium and high OEEI, compared to LCDs with low OEEI (p < 0.05 for both). TUNEL labeling revealed increased quantity of TUNEL-positive apoptotic cells in the higher OEEI groups, relative to the lower group (p < 0.05 for both). Results of the ROS assays showed that ROS production increased significantly (based on relative fluorescence intensity) after exposure to medium and high OEEIs (p < 0.05 for both), with ROS levels correlated to OEEI intensity. LCD exposure was found to induce mitochondrial dysfunction in 661W cells, with LCD exposure to higher OEEIs resulting in a decrease of JC-1 (staining dye) aggregation (associated with healthy cells) and an increase in JC-1 monomers (associated with apoptotic cells). Exposure to LCD led to a significant increase in oxidative stress/inflammatory response-associated protein expression (e.g., intercellular adhesion molecule 1, inducible nitric oxide synthase, heme oxygenase-1), and EMSA findings indicated activation of the NF-κB pathway in the medium and high OEEI groups, relative to the low OEEI group (p < 0.05 for both).

Researchers conclude that LCD exposure-induced photoreceptor damage is indeed linked to LCD energy emission. Results demonstrate that LCDs with higher OEEI is associated with ROS production, apoptosis of retinal cells, upregulation of protein expression associated with inflammatory response, and activation of the NF-κB pathway. Findings suggest that the use of LCDs with lower energy emission may be an effective way to protect against light-induced retinal injury. Potential limitations of the study involve the use of 661W cells, which share only limited features of cone photoreceptors, instead of primary retinal cell culture as the model of retinal damage. Given the relatively short period of light exposure (3 days), further research is also needed to analyze the effects of chronic LCD exposure on retinal health.

Source: Lin C, Yang CM, Yang CH. Effects of the emitted light spectrum of liquid crystal displays on light-induced retinal photoreceptor cell damage. International Journal of Molecular Sciences. 2019; 20: 2318.  DOI: 10.3390/ijms20092318.

© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Posted July 29, 2019.

Angeline A. De Leon, MA, graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. Her specialized area of research involves the complementary use of neuroimaging and neuropsychology-based methodologies to examine how lifestyle factors, such as physical activity and meditation, can influence brain plasticity and enhance overall connectivity.

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