Rapp L M, Ghalayini A J
Cullen Eye Institute, Baylor College of Medicine, Houston, TX, 77030, USA.
Exp Eye Res. 1999 Jun;68(6):757-64. doi: 10.1006/exer.1999.0662.
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 short-wavelength light, and little is known about the initiating events for this damage class. The present study sought to determine the involvement of rhodopsin 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 1500 microW cm-2of UVA light. When animals were placed in darkness following 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 time points, animals were returned to dim cyclic light and by 2 days following exposure, rhodopsin levels had risen to 57% of control. In contrast, opsin levels at this same time point were unaffected by UVA exposure. Other observations indicating the UVA exposure affected photoreceptor cell metabolism included a 27% decrease in the rate of opsin synthesis between 1 and 2 days 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 bleaching of rhodopsin followed by a slow rate of recovery and altered photoreceptor cell metabolism. These results are consistent with the concept that rhodopsin mediates UVA-induced retinal damage and the possible mechanisms by which this might occur are discussed in relation to alternative hypotheses currently in the literature.
有大量证据表明，视紫红质是介导中可见光波长暴露对大鼠视网膜造成光损伤的发色团。然而，短波长光更易导致视网膜损伤，对于此类损伤的起始事件却知之甚少。本研究旨在通过检测色素沉着大鼠眼睛急性暴露于紫外线A（UVA）后早期时间点的视紫红质水平和视蛋白合成，来确定视紫红质漂白在短波长损伤中的作用。在1500微瓦/平方厘米的UVA光照射1小时期间，视紫红质逐渐下降至未暴露对照眼睛水平的8%。在此暴露后将动物置于黑暗中，暴露后2小时视紫红质仅恢复至对照水平的27%，表明再生速率非常缓慢。对于更晚的时间点，将动物放回昏暗的循环光环境中，暴露后2天时，视紫红质水平已升至对照的57%。相比之下，同一时间点的视蛋白水平不受UVA暴露影响。其他表明UVA暴露影响光感受器细胞代谢的观察结果包括：暴露后1至2天视蛋白合成速率下降27%，以及暴露后最初3天视杆外段盘更新速率降低69%。这些数据表明，视网膜中的UVA光应激会导致视紫红质逐渐漂白，随后恢复缓慢且光感受器细胞代谢改变。这些结果与视紫红质介导UVA诱导的视网膜损伤这一概念一致，并结合当前文献中的其他假设讨论了其可能的发生机制。
