Influence of UVA light stress on photoreceptor cell metabolism: Decreased rates of rhodopsin regeneration and opsin synthesis

There is considerable evidence indicating that rhodopsin is the chromophore mediating light damage to the rat retina caused by exposure to mid-visible wavelengths. Retinal damage is, however, more effectively produced by shor t-wavelength light, and little is known about the initiating events for thi s damage class. The present study sought to determine the involvement of rh odopsin bleaching in short-wavelength damage by examining rhodopsin levels and opsin synthesis at early time points following acute ultraviolet-a (UVA ) exposures of the pigmented rat eye. A gradual decline in rhodopsin to 8% of the level in non-exposed control eyes occurred over a 1 hr exposure to 1 500 mu W cm(-2) of UVA light. When animals were placed in darkness followin g this exposure, rhodopsin had recovered to only 27% of control levels by 2 hr post-exposure indicating a very slow rate of regeneration, For later ti me points, animals were returned to dim cyclic light and by 2 days followin g exposure, rhodopsin levels had risen to 57% of control. In contrast, opsi n levels at this same time point were unaffected by UVA exposure. Other obs ervations indicating the UVA exposure affected photoreceptor cell metabolis m included a 27% decrease in the rate of opsin synthesis between 1 and 2 da ys following exposure, and a 69% reduction in the rate of rod outer segment disk renewal during the initial 3 days following exposure. These data show that UVA light stress in the retina causes a gradual bleach ing of rhodopsin followed by a slow rate of recovery and altered photorecep tor cell metabolism, These results are consistent with the concept that rho dopsin mediates UVA-induced retinal damage and the possible mechanisms by w hich this might occur are discussed in relation to alternative hypotheses c urrently in the literature. (C) 1999 Academic Press.