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Blue-light-induced dysfunction of the blood-retinal barrier at the pigment epithelium in albino versus pigmented rabbits.
Exp Eye Res 1994; 58(1):31-40EE

Abstract

The purpose of this study was to determine the role of epithelial melanin in blue light phototoxicity of the retina. The first manifestation of the phototoxicity has been shown to be a breakdown of the blood-retinal barrier at the retinal pigment epithelium. The blood-retinal barrier function of six New Zealand albino rabbits was compared to that of four pigmented chinchilla rabbits after exposure to broad-band blue light (400-520 nm). Additionally, the spectral sensitivity of blood-retinal barrier dysfunction was determined by exposing 15 New Zealand albino rabbits to narrow-band blue light with peak intensity at lambda = 408 nm, 418 nm, 439 nm, 455 nm and 485 nm (bandwidth: 11.7-13.5 nm). The blood-retinal barrier function was evaluated with vitreous fluorophotometry. Ultrastructural changes and permeability of the retinal pigment epithelium for horseradish peroxidase were evaluated in the albino rabbits with electron microscopy. Exposure to broad-band blue light up to 832 J cm-2 demonstrated the blood-retinal barrier of albino and pigmented rabbits to be equally sensitive. Electron microscopy of albino rabbits exposed to above-threshold energy demonstrated an increase of inclusion bodies in the retinal pigment epithelium and vacuolation of the cytoplasm. Transcellular passage of intra-arterially administered horseradish peroxidase through the pigment epithelium into the subretinal space was seen. The narrow-band exposures demonstrated that light of 439 nm was more effective than the light of other wavelengths in inducing barrier dysfunction in albino rabbits. This implies that chromophores absorbing at 439 +/- 6 nm were responsible for the phototoxicity in albino rabbits. The results indicate that melanin does not have a damaging nor a protective role in phototoxicity since (1) the presence of melanin is not essential for blue-light-induced photochemical damage to the blood-retinal barrier at the retinal pigment epithelium, and (2) protection from this sort of damage is not greater in melanin containing epithelia than in non-melanin containing epithelia.

Authors+Show Affiliations

Department of Ophthalmology, Leiden University Hospital, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

8157099

Citation

Putting, B J., et al. "Blue-light-induced Dysfunction of the Blood-retinal Barrier at the Pigment Epithelium in Albino Versus Pigmented Rabbits." Experimental Eye Research, vol. 58, no. 1, 1994, pp. 31-40.
Putting BJ, Van Best JA, Vrensen GF, et al. Blue-light-induced dysfunction of the blood-retinal barrier at the pigment epithelium in albino versus pigmented rabbits. Exp Eye Res. 1994;58(1):31-40.
Putting, B. J., Van Best, J. A., Vrensen, G. F., & Oosterhuis, J. A. (1994). Blue-light-induced dysfunction of the blood-retinal barrier at the pigment epithelium in albino versus pigmented rabbits. Experimental Eye Research, 58(1), pp. 31-40.
Putting BJ, et al. Blue-light-induced Dysfunction of the Blood-retinal Barrier at the Pigment Epithelium in Albino Versus Pigmented Rabbits. Exp Eye Res. 1994;58(1):31-40. PubMed PMID: 8157099.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Blue-light-induced dysfunction of the blood-retinal barrier at the pigment epithelium in albino versus pigmented rabbits. AU - Putting,B J, AU - Van Best,J A, AU - Vrensen,G F, AU - Oosterhuis,J A, PY - 1994/1/1/pubmed PY - 1994/1/1/medline PY - 1994/1/1/entrez SP - 31 EP - 40 JF - Experimental eye research JO - Exp. Eye Res. VL - 58 IS - 1 N2 - The purpose of this study was to determine the role of epithelial melanin in blue light phototoxicity of the retina. The first manifestation of the phototoxicity has been shown to be a breakdown of the blood-retinal barrier at the retinal pigment epithelium. The blood-retinal barrier function of six New Zealand albino rabbits was compared to that of four pigmented chinchilla rabbits after exposure to broad-band blue light (400-520 nm). Additionally, the spectral sensitivity of blood-retinal barrier dysfunction was determined by exposing 15 New Zealand albino rabbits to narrow-band blue light with peak intensity at lambda = 408 nm, 418 nm, 439 nm, 455 nm and 485 nm (bandwidth: 11.7-13.5 nm). The blood-retinal barrier function was evaluated with vitreous fluorophotometry. Ultrastructural changes and permeability of the retinal pigment epithelium for horseradish peroxidase were evaluated in the albino rabbits with electron microscopy. Exposure to broad-band blue light up to 832 J cm-2 demonstrated the blood-retinal barrier of albino and pigmented rabbits to be equally sensitive. Electron microscopy of albino rabbits exposed to above-threshold energy demonstrated an increase of inclusion bodies in the retinal pigment epithelium and vacuolation of the cytoplasm. Transcellular passage of intra-arterially administered horseradish peroxidase through the pigment epithelium into the subretinal space was seen. The narrow-band exposures demonstrated that light of 439 nm was more effective than the light of other wavelengths in inducing barrier dysfunction in albino rabbits. This implies that chromophores absorbing at 439 +/- 6 nm were responsible for the phototoxicity in albino rabbits. The results indicate that melanin does not have a damaging nor a protective role in phototoxicity since (1) the presence of melanin is not essential for blue-light-induced photochemical damage to the blood-retinal barrier at the retinal pigment epithelium, and (2) protection from this sort of damage is not greater in melanin containing epithelia than in non-melanin containing epithelia. SN - 0014-4835 UR - https://www.unboundmedicine.com/medline/citation/8157099/Blue_light_induced_dysfunction_of_the_blood_retinal_barrier_at_the_pigment_epithelium_in_albino_versus_pigmented_rabbits_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4835(84)71192-4 DB - PRIME DP - Unbound Medicine ER -