ENVIRONMENTAL LIGHT AND RETINAL MEMBRANE DEVELOPMENT

强光照射对正常和视网膜营养不良大鼠的影响 将通过测量光引起的杆外部变化来确定 节（ROS）和视网膜色素上皮（RPE）膜脂质， proteins. 为此，已作出合作安排， 通过放射免疫测定法测量来自光暴露的眼睛的ROS中的视蛋白， 从正常和营养不良大鼠中获得在组织培养中生长的RPE细胞。 目前的假设，眼睛光损伤将调查， 将不同年龄大鼠视网膜中的视紫红质含量与 光饲养历史的浓度的氢过氧化物和 抗坏血酸含量，这是已知的，在强光下会改变 exposure. 将收集生物化学和组织学证据， 证实了光暴露的眼睛中视觉细胞死亡的程度， 大鼠 暴露时间、光照强度和光敏剂等变量 短的光暗周期将被研究，因为它们与序列有关 视网膜和RPE中的眼组织破坏， 营养不良的幼鼠对光的极度敏感 研究 将进行视网膜脂质代谢，以评估 感光细胞在光暴露期间修复其膜， 获得插入到光损伤的分子序列中。 一种机械的 ROS过氧化膜破坏的研究计划通过比较 体内过程与体外孵育过程中发生的过程， 光 低龄化、周期性光照饲养和 维生素A缺乏症将被研究，因为它们与视觉细胞损失有关 以及制定防止这一进程的战略， 实验动物 这些研究应该能让我们更好地理解 在光暴露期间视网膜-RPE相互作用的影响， 强单色光对人眼损伤评估 光源。 将这些研究扩展到遗传性失明者 通过外推，视网膜营养不良大鼠具有对人类视网膜的暗示， 遗传性异常

The effects of intense light exposure in normal and retinal dystrophic rats will be determined by measuring light induced changes in the rod outer segment (ROS) and retinal pigment epithelium (RPE) membrane lipids and proteins. To this end, collaborative arrangements have been made to measure opsin by radioimmunoassay in ROS from light exposed eyes and to acquire RPE cells grown in tissue culture from normal and dystrophic rats. Current hypotheses of ocular light damage will be investigated by correlating the rhodopsin content in retinas of rats fo various ages and light rearing histories to the concentrations of hydroperoxides and the ascorbic acid content, which are known to be altered during intense light exposure. Both biochemical and histological evidence will be gathered to substantiate the extent of visual cell death in the light exposed eyes of rats. The variables duration of exposure, light intensity and intermittant short light-dark cycles will be investigated as they relate to the sequence of ocular tissue destruction in the retina and RPE and as they relate to the exquisite sensitivity of young dystrophic rats to light. Studies of retinal lipid metabolism will be performed to assess the ability of the photoreceptor cell to repair its membranes during light exposure and to gain insites into the molecular sequence of light damage. A mechanistic study of ROS peroxidative membrane destruction is planned by comparisons of the in vivo process with that which occurs during in vitro incubation in light. The prophylactic effects of young age, cyclic light rearing and vitamin A deficiency will be studied as they relate to visual cell loss from light and in the development of strategies to prevent that process in experimental animals. These studies should lead to a better understanding of retina-RPE interactions during light exposure and have implications in the assessment of ocular light damage in humans from intense monochromatic light sources. The extension of these studies to the genetically blind retinal dystrophic rat has implication, by extrapolation, to human retinal abnormalities of a genetic nature.