ENVIRONMENTAL LIGHT AND RETINAL MEMBRANE DEVELOPMENT

建议继续进行研究，并扩大与 可见光对视网膜光感受器细胞的病理影响 大鼠视网膜色素上皮(RPE)我们将研究这一机制 通过确定抗氧化剂的时间序列来控制光损伤 光分离的杆状外节(ROS)中的酶失活 暴露大鼠和ROS膜中二十二碳六烯酸的损失。这个 抗坏血酸对ROS酶和血脂的保护作用 连续光照或短光暗暴露的正常大鼠的测量 在接下来的黑暗时期和在不同时间分离的ROS中 曝光量。ROS膜的过氧化作用将作为 光暴露的致因因素。ROS膜的过氧化将是 通过测量光损伤的程度来检验其作为光损伤的原因 黄斑变性大鼠视网膜视紫质丢失和过氧化氢蓄积的研究 在他们的ROS中耗尽了二十二碳六烯酸。的保护作用 减少的ROS二十二碳六烯酸和抗坏血酸将对光伤害 在大鼠身上进行联合检查，目的是进一步减少，或 消除对视网膜的轻微损伤。同样的实验范式 光曝光将被用来确定光感受器的序列 细胞和RPE细胞膜受损。因为不同国家的 周期光之间光对感光细胞和RPE细胞的损伤程度 和黑暗饲养的正常大鼠和年轻和老年营养不良的大鼠这些将 做我们的实验动物。我们将确定RPE细胞的范围 分离RPE质膜参与光损伤过程中的膜损伤 并测量膜酶和脂类。既有玻璃珠子，也有绑珠子 针对RPE质膜蛋白的单抗将用于 从光损伤的大鼠身上分离出膜。相关光和 将对受损的眼睛进行电子显微镜检查 老鼠。我们将通过合作安排提供单抗 RPE质膜蛋白在正常人和正常人中的功能研究 组织培养中营养不良的大鼠视网膜色素上皮细胞。我们在时间上的研究 大鼠视网膜及视网膜与视网膜色素上皮之间的光损伤顺序 将提供对该模型中的光损伤机制的深入了解 可以扩展到抗坏血酸也被显示出来的坏血酸动物 是为了保护自己。这些研究被视为与 预防对人眼的光损害，特别是在 在外科手术中随着频率的增加而发生的强烈光暴露 设置和工作场所。

Studies are proposed to continue and extend findings relevant to the pathological effects of visible light in retinal photoreceptor cells and in the retinal pigment epithelium (RPE) of rats. We will study the mechanism of light damage by determining the temporal sequence of antioxidative enzyme inactivation i n rod outer segments (ROS) isolated from light exposed rats and the loss od docosahexaenoic acid from ROS membranes. The protective effect of ascorbic acid on ROS enzymes and lipids will be measured in normal rats exposed to continuous light or to short light-dark periods and in ROS isolated at various times in the dark period following light exposure. Peroxidation of ROS membranes will be examined as the causative factor of light exposure. Peroxidation of ROS membranes will be examined as the causative factor of light damage by measureing the extent of rhodopsin loss and peroxide accumulation in the retinas of rats with depleted docosahexaenoic acid in their ROS. The protective effects of reduced ROS docosahexaenoate and ascorbate against light damage will be examined in combination, in rats, with the aim of further reducing, or eliminating, light damage to the retina. The same experimental paradigm of light exposures will be used to determine the sequence of photoreceptor cell and RPE cell membrane damage. Because of the differences in the extent of photoreceptor and RPE cell damage from light between cyclic light and dark reared normal rats and young and older dystrophic rats these will be our experimental animals. We will determine the extent of RPE cell membrane involvement during light damage by isolating RPE plasma membranes and measuring membrane enzymes and lipids. Both glass beads and bead-bound monoclonal antibodies against RPE plasma membrane proteins will be used to isolate the membranes from light damaged rats. Correlative light and electron microscopic studies will be performed on the eyes of light damaged rats. We will supply monoclonal antibodies by collaborative arrangement to begin functional studies of RPE plasma membrane protiens in normal and dystrophic rat RPE cells in tissue culture. Our studies in the temporal sequence of light damage in retina and between retina and RPE in the rat will provide insights into the mechanism of light damage in this model and can be extended to scorbutic animals in which ascorbate has also been shown to be protective. These studies are seen as being relevant to the prevention of light damage in the human eye, especially during periods of intense light exposure as occurs with increasing frequency in surgical settings and in the work place.