Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 20 (9)

Effects of the Emitted Light Spectrum of Liquid Crystal Displays on Light-Induced Retinal Photoreceptor Cell Damage

Affiliations

Effects of the Emitted Light Spectrum of Liquid Crystal Displays on Light-Induced Retinal Photoreceptor Cell Damage

Chao-Wen Lin et al. Int J Mol Sci.

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.

Keywords: NF-κB; blue light; light spectrum; light-emitting diodes (LED); liquid crystal display (LCD); oxidative stress; photo-injury; photoreceptor.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Viability of 661W cells exposed to liquid crystal displays with different luminance for 1, 2, and 3 days. Cell viability was analyzed using alamarBlue assays. Ctrl: control group, no light exposure; All data represent the means ± SD. * p < 0.05 compared to data on day 1 using two-way analysis of variance (ANOVA) with post hoc Dunnett’s multiple comparisons test; n = 16 per group.
Figure 2
Figure 2
Viability of 661W cells exposed to liquid crystal displays with different ocular energy exposure index (OEEI) values for 3 days. Cell viability was analyzed using alamarBlue assays. Ctrl: control group, no light exposure; All data represent the median and the interquartile range. * p < 0.05 compared to the low OEEI group using the Kurskal-Wallis test with post hoc Dunn test; n = 12 per group.
Figure 3
Figure 3
Apoptotic cells detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotinide end labeling (TUNEL) in 661W cells. (A) Representative images of 661W cell apoptosis in controls and cells exposed to liquid crystal display (LCD) with low, medium, and high ocular energy exposure index for 24 h. Ctrl: control group, no light exposure; bar = 200 μm. (B) Number of TUNEL-positive cells was counted in at least four randomly chosen views, represented as columns. Ctrl: control group, no light exposure; All data represent the median and the interquartile range. * p < 0.05 compared to the control group using the Kurskal-Wallis test with post hoc Dunn test; n = 3 in each group.
Figure 4
Figure 4
Reactive oxygen species assay in 661W cells after exposure to liquid crystal display (LCD) with different ocular energy exposure index (OEEI) for 3 days. (A) 2′,7′-dichlorodihydrofluorescein diacetate (H2DCFDA) was added to 661W cells after exposure to LCD with low, medium, and high OEEI. The images were captured by florescence microscopy. Bar = 100 μm. (B). Quantitative analysis of the images obtained from fluorescence microscopy using image-processing software (Image-J). Fluorescence level in the control group was arbitrarily set as 1. Ctrl: control group, no light exposure; All data represent the median and the interquartile range. * p < 0.05 compared to the control group by Kurskal-Wallis test with post hoc Dunn test; n = 3 in each group.
Figure 5
Figure 5
Liquid crystal display (LCD) exposure induces mitochondrial dysfunction in 661W cells. (A) 661W cells were subjected to JC-1 staining, which was analyzed using florescence microscopy. J-aggregates and JC-1 monomers were detected with settings designed to detect Texas Red and FITC, respectively. The 3-day exposure to LCD decreased JC-1 aggregation and increased JC-1 monomers in 661W cells. The effect was stronger in LCDs with higher ocular energy exposure index (OEEI). Bar = 100 μm. (B) Green/Red-fluorescence (+) cell ratio (%). The numbers of cells (red or green-stained cells) were counted using image processing software (Image-J). Ctrl: control group, no light exposure; All data represent the median and the interquartile range. * p < 0.05 compared to the control group by Kurskal-Wallis test with post hoc Dunn test; n = 4 in each group.
Figure 6
Figure 6
Liquid crystal display (LCD) exposure increases oxidative stress and inflammatory-related protein expression levels in 661W cells. (A) Evaluation of the protein expression of enzymes associated with inflammatory response by western blot analysis. 661W cells were exposed to LCD with low, medium, and high ocular energy exposure index (OEEI) for 3 days. GAPDH was used as the internal control. C: control group, no light exposure; L: low, M: medium, H: high OEEI. (B) Relative expression of intercellular adhesion molecule 1 (ICAM-1), inducible nitric oxide synthase (iNOS), monocyte chemoattractant protein 1 (MCP-1), and heme oxygenase-1 (HO-1). Ctrl: control group, no light exposure; All data represent the median and the interquartile range. * p < 0.05 compared to the control group by Kurskal-Wallis test with post hoc Dunn test; n = 5 per group.
Figure 7
Figure 7
Exposure to liquid crystal display (LCD) with medium and high ocular energy exposure index (OEEI) increases cleaved caspase-3 expression in 661W cells. 661W cells were exposed to LCD with low, medium, and high OEEI for 3 days. The caspase-3 expression levels were analyzed by western blot. In medium and high OEEI groups, the cleavage forms of caspse-3 were obviously observed (arrow).
Figure 8
Figure 8
Exposure to liquid crystal display (LCD) with higher ocular energy exposure index (OEEI) activates the nuclear factor-κB (NF-κB) pathway. (A) Electrophoretic mobility shift assay (EMSA) was used to evaluate the DNA-binding activity of NF-κB in 661W cells after exposure to LCD with low, medium, and high OEEI for 3 days. Adding a 100-fold molar excess of unlabeled NF-κB probe completely inhibited the binding of labeled probe to the NF-κB /DNA complex. Lane 1: p50 subunit of NF-κB; Lane 2: free probe; Lane 3: control group, no light exposure; Lane 4: Low OEEI group; Lane 5: medium OEEI group; Lane 6: high OEEI group; Lane 7: competition with 100x unlabeled NF-κB probe; Lane 8: anti-p65 antibody supershift band. (B) Quantification of EMSA results. Expression level in the control group was arbitrarily set as 1. Ctrl: control group, no light exposure; All data represent the median and the interquartile range. * p < 0.05 compared to the low OEEI group using Kurskal-Wallis test with post hoc Dunn test; n = 3 in each group.
Figure 9
Figure 9
Schematic diagram of 661W cells seeded on a 24-well plate with the exposure of liquid crystal displays (LCD).
Figure 10
Figure 10
Visible light spectra of liquid crystal displays (LCDs) with low, medium, and high ocular energy exposure index (OEEI) values.

Similar articles

See all similar articles

References

    1. Holzman D.C. What’s in a color? The unique human health effect of blue light. Environ. Health Perspect. 2010;118:A22–A27. doi: 10.1289/ehp.118-a22. - DOI - PMC - PubMed
    1. Stevens R.G., Brainard G.C., Blask D.E., Lockley S.W., Motta M.E. Adverse health effects of nighttime lighting. Am. J. Prev. Med. 2013;45:343–346. doi: 10.1016/j.amepre.2013.04.011. - DOI - PubMed
    1. Tso M.O. Photic maculopathy in rhesus monkey. A light and electron microscopic study. Investig. Ophthalmol. 1973;12:17–34. - PubMed
    1. Parver L.M., Auker C.R., Fine B.S. Observations on monkey eyes exposed to light from an operating microscope. Ophthalmolgy. 1983;90:964–972. doi: 10.1016/S0161-6420(83)80024-4. - DOI - PubMed
    1. Ham W.T., Jr., Mueller H.A., Sliney D.H. Retinal sensitivity to damage from short wavelength light. Nature. 1976;260:153–155. doi: 10.1038/260153a0. - DOI - PubMed
Feedback