Spectral transmittance of the rat lens

Gorgels, Theo G. M. F.; Norren, Dirk van

doi:10.1016/0042-6989(92)90206-x

Cited by 40 publications

(28 citation statements)

References 10 publications

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“…a Non-exposed (0.126 t EDC); b 3 kJ/m 2 (0.185 t EDC); c 5 kJ/m 2 (0.311 t EDC); d 8 kJ/m 2 (0.347 t EDC); e 14 kJ/m 2 (0.703 t EDC) cornea at this wavelength is low, but not zero. In vitro measurements of corneal transmission vary from`2% [6] to 20% [14] for the rat, 9% [3] for the human and 24% [2] for the rabbit. The small fraction of the UVR that reaches the lens is strongly absorbed by the lens [2,3] and probably damages the lens directly.…”

Section: Discussionmentioning

confidence: 99%

Dose-response function for lens forward light scattering after in vivo exposure to ultraviolet radiation

Michael

Söderberg

Chen

1998

Graefe's Archive for Clinical and Experimental Ophthalmology

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Section: Discussionmentioning

confidence: 99%

Dose-response function for lens forward light scattering after in vivo exposure to ultraviolet radiation

Michael

Söderberg

Chen

1998

Graefe's Archive for Clinical and Experimental Ophthalmology

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“…We converted the photometric intensities to physiological quantal fluxes for the murine eye, following Lyubarsky and Pugh (1996) and Pugh (1998) and recognizing that 1 cd /m 2 ϭ lux for an extended Ganzfeld source. Transmissivity of the rodent lens (Gorgels and van Norren, 1992) is ϳ1.6 times greater than the human lens (Wyszecki and Stiles, their Table 2.4.6) for ϭ 500 nm. Using these factors in the conversion schema above, an ERG Ganzfeld stimulus of 2800°K with surface luminance of 1 cd /m 2 (at ϭ 500 nm) yields 2575 photoisomerizations rod Ϫ1 sec Ϫ1 (Rh* rod Ϫ1 sec Ϫ1 ) for the mouse.…”

Section: Methodsmentioning

confidence: 99%

Constitutive “Light” Adaptation in Rods from G90D Rhodopsin: A Mechanism for Human Congenital Nightblindness without Rod Cell Loss

et al. 2001

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A dominant form of human congenital nightblindness is caused by a gly903asp (G90D) mutation in rhodopsin. G90D has been shown to activate the phototransduction cascade in the absence of light in vitro. Such constitutive activity of G90D rhodopsin in vivo would desensitize rod photoreceptors and lead to nightblindness. In contrast, other rhodopsin mutations typically give rise to nightblindness by causing rod cell death. Thus, the proposed desensitization without rod degeneration would be a novel mechanism for this disorder. To explore this possibility, we induced mice to express G90D opsin in their rods and then examined rod function and morphology, after first crossing the transgenic animals with rhodopsin knock-out mice to obtain appropriate levels of opsin expression. The G90D mouse opsin bound the chromophore and formed a bleachable visual pigment with max of 492 nm that supported rod photoresponses. (Gϩ/Ϫ, Rϩ/Ϫ) retinas, heterozygous for both G90D and wildtype (WT) rhodopsin, possessed normal numbers of photoreceptors and had a normal rhodopsin complement but exhibited considerable loss of rod sensitivity as measured electroretinographically. The rod photoresponses were desensitized, and the response time to peak was faster than in (Rϩ/Ϫ) animals. An equivalent desensitization resulted by exposing WT retinas to a background light producing 82 photoisomerizations rod Ϫ1 sec Ϫ1 , suggesting that G90D rods in darkness act as if they are partially "light-adapted." Adding a second G90D allele gave (Gϩ/ϩ, Rϩ/Ϫ) animals that exhibited a further increase of equivalent background light level but had no rod cell loss by 24 weeks of age. (Gϩ/ϩ, RϪ/Ϫ) retinas that express only the mutant rhodopsin develop normal rod outer segments and show minimal rod cell loss even at 1 year of age. We conclude that G90D is constitutively active in mouse rods in vivo but that it does not cause significant rod degeneration. Instead, G90D desensitizes rods by a process equivalent to light adaptation.

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“…The photosensitivity of rhodopsin to bleaching by UVA light is not known but rhodopsin absorbs UVA light as a result of its ' cis ' peak at 354 nm which absorbs at about one-third its primary peak (Stark and Tan, 1982). Furthermore, transmittance through the rat lens in the UVA ranges from 35 to 79 % between 325 and 400 nm which is much greater than in primates (Gorgels and van Norren, 1991). These considerations suggest that UVA light is capable of bleaching rhodopsin but at a slower rate than for mid-visible wavelengths which was indicated by the present finding of a gradual decrease in rhodopsin levels during the 1 hr UVA exposure.…”

Section: Discussionmentioning

confidence: 94%

Influence of UVA Light Stress on Photoreceptor Cell Metabolism: Decreased Rates of Rhodopsin Regeneration and Opsin Synthesis

Rapp

Ghalayini

1999

Experimental Eye Research

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Spectral transmittance of the rat lens

Cited by 40 publications

References 10 publications

Dose-response function for lens forward light scattering after in vivo exposure to ultraviolet radiation

Dose-response function for lens forward light scattering after in vivo exposure to ultraviolet radiation

Constitutive “Light” Adaptation in Rods from G90D Rhodopsin: A Mechanism for Human Congenital Nightblindness without Rod Cell Loss

Influence of UVA Light Stress on Photoreceptor Cell Metabolism: Decreased Rates of Rhodopsin Regeneration and Opsin Synthesis

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