• Corpus ID: 23617758

Protective effect of halothane anesthesia on retinal light damage: inhibition of metabolic rhodopsin regeneration.

@article{Keller2001ProtectiveEO,
  title={Protective effect of halothane anesthesia on retinal light damage: inhibition of metabolic rhodopsin regeneration.},
  author={Caroline Gubser Keller and Christian Grimm and Andreas Wenzel and Farhad Hafezi and Charlotte E. Remé},
  journal={Investigative ophthalmology \& visual science},
  year={2001},
  volume={42 2},
  pages={
          476-80
        }
}
PURPOSE To determine whether the volatile anesthetic halothane protects against light-induced photoreceptor degeneration in the rodent retina. METHODS Albino mice and rats were anesthetized with halothane and exposed to high levels of white or blue light. Nonanesthetized animals served as controls. Retinal morphology was assessed by light microscopy, and apoptosis of photoreceptor cells was verified by detection of fragmented genomic DNA and in situ staining of apoptotic nuclei (TUNEL assay… 

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References

SHOWING 1-10 OF 31 REFERENCES

Blue light's effects on rhodopsin: photoreversal of bleaching in living rat eyes.

PURPOSE To determine whether blue light induces photoreversal of rhodopsin bleaching in vivo. METHODS Eyes of anesthetized albino rats were exposed to either green (550 nm) or deep blue (403 nm)

Protection of Rpe65-deficient mice identifies rhodopsin as a mediator of light-induced retinal degeneration

The transcription factor AP-1, a central element in the apoptotic response to light, is not activated in the absence of rhodopin, indicating that rhodopsin is essential for the generation or transduction of the intracellular death signal induced by light.

The Rpe65 Leu450Met Variation Increases Retinal Resistance Against Light-Induced Degeneration by Slowing Rhodopsin Regeneration

It is found that, in contrast to previous assertions, LDS does not correlate with the maximal retinal content of rhodopsin present after dark adaptation, and correlated positively with the kinetics of r Rhodopsin regeneration, which determine rhodopin availability during light exposure.

Retinal damage by light in rats.

The retina of laboratory rats is affected irreversibly by intense light applied for less than 1 hour or for up to 2 days depending upon experimental conditions, and the action spectrum of the daviaging effect approximated that of visual excitation as measured by the ERG.

Light-induced acceleration of photoreceptor degeneration in transgenic mice expressing mutant rhodopsin.

It is suggested that light activation of rhodopsin contributes to the severity of the degenerative disease resulting from the P23H opsin mutation, and the possibility that minimizing exposure to light may help to prolong useful vision of patients with this form of retinitis pigmentosa is raised.

The absence of c-fos prevents light-induced apoptotic cell death of photoreceptors in retinal degeneration in vivo

It is found that following dark adaptation and two hours of light exposure both groups of animals exhibited only a few apoptotic cells, however, at 12 and 24 additional hours after light exposure, apoptosis increased dramatically in controls but was virtually absent in those mice lacking c-fos, suggesting c- fos is essential for light-induced apoptosis of photoreceptors.

Strain differences in sensitivity to light-induced photoreceptor degeneration in albino mice.

The findings demonstrate that different inbred strains of a given species may exhibit a wide range of sensitivities to constant light exposure and that most albino mouse strains examined thus far are highly sensitive to the damaging effects of light.

Light-induced apoptosis: differential timing in the retina and pigment epithelium.

A new in vivo model system will allow measurement of dose-responses, a potential spectral dependence and the molecular background of apoptotic mechanisms in the retina, and observed that the timing of apoptosis in the photoreceptors and pigment epithelium was remarkably different.

Increased susceptibility to constant light in nr and pcd mice with inherited retinal degenerations.

The present data add to other experimental evidence suggesting that photoreceptors already undergoing inherited or other forms of degeneration may be particularly susceptible to the damaging effects of excessive light.

Action spectrum of retinal light-damage in albino rats.

Retinal light damage in the albino rat under these conditions was rhodopsin mediated, and proper assessment of the extent of damage could only be made by some method that integrates over the entire retinal section.