Abstract

Blue light-induced phototoxicity plays an important role in retinal degeneration and might cause damage as a consequence of smartphone dependency. Here, we investigated the effects of periodic exposure to blue light-emitting diode in a cell model and a rat retinal damage model. Retinal pigment epithelium (RPE) cells were subjected to blue light in vitro and the effects of blue light on activation of key apoptotic pathways were examined by measuring the levels of Bcl-2, Bax, Fas ligand (FasL), Fas-associated protein with death domain (FADD), and caspase-3 protein. Blue light treatment of RPE cells increased Bax, cleaved caspase-3, FasL, and FADD expression, inhibited Bcl-2 and Bcl-xL accumulation, and inhibited Bcl-2/Bax association. A rat model of retinal damage was developed with or without continuous or periodic exposure to blue light for 28 days. In this rat model of retinal damage, periodic blue light exposure caused fundus damage, decreased total retinal thickness, caused atrophy of photoreceptors, and injured neuron transduction in the retina.

Original languageEnglish
Pages (from-to)196-210
Number of pages15
JournalToxicological Sciences
Volume157
Issue number1
DOIs
Publication statusPublished - May 1 2017

Fingerprint

Smartphones
Retina
Luminance
Apoptosis
Light
Fas-Associated Death Domain Protein
Rats
Fas Ligand Protein
Retinal Pigments
Retinal Pigment Epithelium
Caspase 3
Proteins
Phototoxic Dermatitis
Retinal Degeneration
Neurons
Light emitting diodes
Smartphone
Atrophy
Chemical activation
Association reactions

Keywords

  • Age-related macular degeneration
  • Apoptosis
  • Bax
  • Bcl-2
  • Blue light
  • Caspase-3
  • FasL

ASJC Scopus subject areas

  • Toxicology

Cite this

Periodic exposure to smartphone-mimic low-luminance blue light induces retina damage through Bcl-2/BAX-dependent apoptosis. / Lin, Cheng Hui; Wu, Man Ru; Li, Ching Hao; Cheng, Hui Wen; Huang, Shih Hsuan; Tsai, Chi Hao; Lin, Fan Li; Ho, Jau Der; Kang, Jaw Jou; Hsiao, George; Cheng, Yu Wen.

In: Toxicological Sciences, Vol. 157, No. 1, 01.05.2017, p. 196-210.

Research output: Contribution to journalArticle

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