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Charlotte Keller, Christian Grimm, Andreas Wenzel, Farhad Hafezi, Charlotte E. Remé; Protective Effect of Halothane Anesthesia on Retinal Light Damage: Inhibition of Metabolic Rhodopsin Regeneration. Invest. Ophthalmol. Vis. Sci. 2001;42(2):476-480.
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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). Rhodopsin regeneration after bleaching was determined by
measuring rhodopsin levels in retinas of mice or rats at different time
points in darkness.
results. Halothane anesthesia reversibly inhibited metabolic rhodopsin
regeneration and thus prevented rhodopsin from absorbing high numbers
of photons during light exposure. Consequently, photoreceptors of mice
and rats anesthetized with halothane were completely protected against
degeneration induced by white light. In remarkable contrast, however,
halothane anesthesia did not protect against blue-light–induced
photoreceptor cell death.
conclusions. After the initial bleach, halothane impeded photon absorption by
rhodopsin by inhibiting metabolic rhodopsin regeneration. Apparently,
the rhodopsin-mediated uptake of the critical number of photons to
initiate white light–induced retinal degeneration was prevented. In
contrast, halothane did not protect the retina against blue light. Blue
light can efficiently restore functional rhodopsin from bleaching
intermediates through a process termed photoreversal of bleaching. This
process does not depend on the visual cycle via the pigment epithelium
but nevertheless enables rhodopsin molecules to absorb the critical
number of photons required to induce retinal
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