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The human eyes are gradually adapting to natural light sources as it evolves naturally. But in just 100 years, human technology has been changing with each paing day, and various artificial light sources have been produced. These new artificial light sources will produce quite a lot of blue light, such as Blu-ray accounts for 26% of the light from energy-saving and increasingly popular compact fluorescent lamps. It also includes smartphones, computers, TVs, etc.
The eye is subject to injury from both long-term exposure to blue light and man-made optical . g in the most energetic portion of the visible spectrum, blue light has the greatest potential to induce the photo damage that may ultimately be a factor in retinal disorders such as age-related macular degeneration (AMD).Blue light can cause damage to both photoreceptor and RPE cells in primates.Cumulative exposure to light in the 380 nm to 500 nm range can activate all-ns-retinal accumulated in the photoreceptor outer segments (Figure 1). This blue light photoactivation of all-ns-retinal can induce production of reactive oxygen species (ROS), such as singlet oxygen, hydrogen peroxide, and other free radicals, in the photoreceptor outer segments.
The ROS attack many molecules, including polyunsaturated fatty acids, a major component of cell membranes. The large concention of cell membranes in the retina es it highly sensitive to oxidative stre.In particular,this stre may disrupt the membranous structures of the photoreceptor outer segments, causing incomplete phagocytosis and digestion of oxidized outer segments in the RPE.The consequence is an accumulation of the product lipofuscin in RPE cell granules. In the eye, lipofuscin, also known as “the age pigment,” exposure accumulates over the years and builds up at a faster rate in some retinal diseases. Composed of lipids, proteins, anda number of chromophores, lipofuscin is highly susceptible to photo changes that can produce permanent cellular damage.
The greatest damage followed exposure to the four 10-nm sub-bands within the blue-violet spectrum between 415 nm and 455 nm. In those test cells, morphological changes to RPE cells (cell rounding, lo of confluence, and a decrease in density) were observed 6 hours after exposure (Figure 2).22In addition to wavelength dependence, the toxic effect was A2E-dose-dependent, with the greatest apoptosis rates occurring with 20μM and 40μM concentions of A2E.In cells exposed to the narrow band of blue-violet light centered on 440 nm,though, there was a significant increase in apoptosis, even with 12.5μM A2E, indicating the phototoxicity of those wavelengths.
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