Removal of the blue component of light significantly decreases retinal damage after high intensity exposure

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From: PLoS ONE(Vol. 13, Issue 3)
Publisher: Public Library of Science
Document Type: Report
Length: 7,779 words
Lexile Measure: 1320L

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Author(s): Javier Vicente-Tejedor 1,2,*, Miguel Marchena 1, Laura Ramírez 1, Diego García-Ayuso 3,4, Violeta Gómez-Vicente 5, Celia Sánchez-Ramos 2, Pedro de la Villa 1, Francisco Germain 1

Introduction

Light is converted into useful visual information in the retina. Photoreceptor cells express light-sensitive pigments that absorb photons, initiating a chemical cascade of events known as phototransduction that culminates in the generation of electrical signals. There are three classes of retinal cells that contain visual pigments and are thus responsive to light: the classic photoreceptors, rods and cones, and the intrinsically-photosentitive retinal ganglion cells (ipRGCs). Rods and cones contain rhodopsin and cone opsins respectively, allowing visual perception and color distinction, whereas ipRGCs contain melanopsin and are involved in the entrainment of the circadian rhythms [1,2].

In the mouse retina, rods (502 nm) are more abundant, while cones constitute 2.7-3% of the photoreceptors [3,4]. In contrast to primates, the murine retina has only two spectral cone types: short (S) cones are sensitive to short wavelengths in the ultraviolet (UV) spectrum (359 nm, short wave (SW)), while long/medium (L/M) cones are sensitive to middle-to-long wavelengths (508 nm, medium wave (MW) and long wave (LW)) [5]. In the mouse retina, topographic separation of different classes of cones has been reported [6]. Variations in retinal topography of S and L/M cones have been observed among different strains (albino and pigmented mice) [7]. In addition, five morphological types of ipRGCs have been identified in mice and rats. These cells have diverse functional roles in non-imaging forming vision and in pattern vision [8,9]. Distinct absorbance spectrum in the different photoreceptor cells is due to apoproteins [10]. These opsins provide specific environment for the absorption of light at particular wavelengths [11]. A protonated Schiff base links opsin and chromophore (retinal), producing a spectral shift from ultraviolet (cromophore: maximal absorption 380 nm) to visible light [12]. However, the S cone cromophore is unprotonated and, consequently, is not capable of such spectral shift (<450 nm) [13].

It has been shown that excessive exposure to visible light can cause toxicity in the vertebrate retina [14]. The degree of damage depends on the level of retinal irradiance, wavelength and exposure duration [15,16]. In this regard, the same visible radiation that activates phototransduction is the responsible for causing damage in photosensitive cells [14].

Phototoxicity related retinal damage has been classified into two groups depending on variables such as the incident wavelength, the exposure time and the cell type affected. Class I takes place after long periods of exposure (days to weeks) to low irradiances and the cells affected are the photoreceptors whose wavelengths are activated [14]. Class II occurs after a short exposure (minutes to hours) to high irradiances of white light and the damage is at level of the retinal pigmented epithelium (RPE) [17]. This effect is also known as "blue-light" damage and has been reported for living animals, either anesthetized [18] or free-running [19].

It has been documented that light causes apoptotic death of photoreceptors and RPE cells [20]. Since light bleaches...

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Gale Document Number: GALE|A531127150