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Light‐induced Damage to the Retina: Role of Rhodopsin Chromophore Revisited
Author(s) -
Różanowska Małgorzata,
Sarna Tadeusz
Publication year - 2005
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1562/2004-11-13-ir-371
Subject(s) - rhodopsin , retina , retinal , visual phototransduction , phototoxicity , chromophore , opsin , retinoid , chemistry , biophysics , biochemistry , biology , photochemistry , in vitro , retinoic acid , neuroscience , gene
The presence of the regenerable visual pigment rhodopsin has been shown to be primarily responsible for the acute photo‐damage to the retina. The photoexcitation of rhodopsin leads to isomerization of its chromophore 11‐ cis ‐retinal to all‐ trans‐ retinal (ATR). ATR is a potent photosensitizer and its role in mediating photodamage has been suspectéd for over two decades. However, there was lack of experimental evidence that free ATR exists in the retina in sufficient concentrations to impose a risk of photosensitized damage. Identification in the retina of a retinal dimer and a pyridinium bisretinoid, so called A2E, and determination of its biosynthetic pathway indicate that substantial amounts of ATR do accumulate in the retina. Both light damage and A2E accumulation are facilitated under conditions where efficient retinoid cycle operates. Efficient retinoid cycle leads to rapid regeneration of rhodopsin, which may result in ATR release from the opsin “exit site” before its enzymatic reduction to all‐ trans ‐retinol. Here we discuss photodamage to the retina where ATR could play a role as the main toxic and/or phototoxic agent. Moreover, we discuss secondary products of (photo)toxic properties accumulating within retinal lipofuscin as a result of ATR accumulation.