Written by Angeline A. De Leon, Staff Writer. Blue light-induced phototoxicity, a consequence of smartphone dependency, caused retinal damage in a rat model.

headache - painWith the increasing trend of dependency on smartphones and other mobile devices, the risk of screen-induced vision problems, such as eye fatigue and reduced visual sensitivity, is more prevalent than ever at the population level. The short-wavelength blue light (from 450 to 495 nm) emitted from the screens of smartphones, tablets, and laptops is considered high-energy radiation and is recognized as a risk factor for retinal injury and other potential eye diseases, such as age-related macular degeneration (AMD, an incurable condition associated with vision loss)1. In fact, reports predict the number of AMD cases to increase exponentially until at least 2020 2. More so than white or green light, blue light has been found to generate reactive oxygen species (ROS) in retinal cells 3, triggering an inflammatory response that leads to death of retinal pigment epithelium (RPE) cells and photochemical damage of retinal tissue 4. Animal studies report that even short periods of blue light exposure increase levels of apoptosis-inducing factors (associated with cell death) in retinal cells 5, causing potentially irreversible morphological changes such as loss of photoreceptor segments and pigment epithelium degeneration 6. Given the need to better understand the long-term effects of blue light-induced phototoxicity caused by use of electronics, researchers at the Taipei Medical University (2017) investigated the mechanisms involved in blue-light-induced RPE cell apoptosis in both a cell model and rat model of retinal damage.

To determine the phototoxic effects of blue visible light in the cell model, a blue LED electronic system was inserted inside a cell culture incubator. Human RPE cells were periodically exposed (0, 3, 6, and 12 hours of exposure) to blue light (460 nm, 80 lux) in vitro, and the activation of apoptotic pathways was studied by measuring levels of regulator proteins known to control cell death [Bcl-2, Bax, Fas ligand (FasL), Fas-associated protein with death domain (FADD), and caspase-3 protein]. In the rat model of retinal damage, a total of 16 male Brown Norway rats were divided into four groups and subjected to 0 (control), 0.5, 1, or 3 hours of periodic in vivo blue light exposure for 28 days. Rats were then anaesthetized and their eyes assessed for retinal damage (involving examination of blood vessels in eyes, imaging of inner retina, and measuring thickness of retinal neuron layer).

Periodic blue light treatment was found to have a cytotoxic effect on RPE cells based on significant loss of cell viability (the number of healthy cells in a sample) observed after six hours of blue light exposure, as well as decreased mRNA expression of Bcl-2 (apoptosis suppressor) (p < 0.05) and increased mRNA expression of Bax (apoptosis activator) following 12 hours of treatment. Blue light exposure was also associated with induction of the Bax/Bcl-2 pathway (Bax protein levels increased significantly following 48 hours of blue light exposure, p < 0.05; Bcl-2 protein levels decreased significantly as early as 24 hours following exposure, p < 0.05), Fas/FasL pathway (FasL and FADD protein levels increased significantly after 48 hours of exposure, starting as early as 12 hours, p < 0.05), and caspase cascades (involved in execution phase of apoptosis) (pro caspase-8 protein levels showed significant increase after 48 hours of exposure, p < 0.05) in RPE cells. Analysis of the rat model of retinopathy revealed that periodic blue light exposure was associated with fundus damage (damage on the interior surface of the eye) based on leakage of fluorescein angiography dye in rats exposed to 1 hour (3.02 +/- 0.52-fold on Day 14, 4.29 +/- 0.89-fold on Day 28) and 3 hours (2.59 +/- 1.16-fold on Day 14 and 19.92 +/- 3.88-fold on Day 28) of daily blue light treatment vs. controls (p < 0.05 for both groups on both days). Results also showed that relative to the control condition, daily exposure to 3 hours of blue light for 14 and 28 days was associated with decreased total retinal thickness (p < 0.5 for both days). Finally, after 28 days, periodic 1-hour and 3-hour daily blue light treatment sessions were found to be linked to photoreceptor atrophy based on significantly lower photoreceptor nuclei count, relative to controls (p < 0.05 for both days).

Taken together, findings support a strong correlation between low luminance blue light exposure from electronic screen use and retinal degeneration, emphasizing the risk of irreversible retinopathy through blue light-induced cell death. Long-term exposure to electronic screens remains a global issue and a health risk that should be carefully managed, especially in the coming years.

Source: Lin CH, Wu MR, Li CH, et al. Periodic exposure to smartphone-mimic low-luminance blue light induces retina damage through Bcl-2/BAX-dependent apoptosis. Toxicological Sciences. 2017; 157(1): 196-210. DOI:10.1093/toxsci/kfx030.

© The Author 2017. Published by Oxford University Press on behalf of the Society of Toxicology.

Posted July 17, 2018.

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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