Defense mechanism for retinal light damage.

锰超氧化物歧化酶（Mn-SOD）是一种天然存在的活性氧中间体清除剂。我们假设Mn-SOD表达的增强可能是一种防御氧化挑战的机制，即强光暴露。我们研究了光致视网膜损伤后Mn-SOD表达增加的可能性。大鼠在80勒克斯的循环光下暴露2周，然后在1800勒克斯的强光下暴露24小时，然后返回循环光。取光刺激后14 d的大鼠和对照大鼠的眼睛，用兔抗大鼠Mn-SOD血清免疫组化检测蛋白表达。外核层萎缩的光暴露组与对照组之间无显著差异。光激后第1、7、14天，实验动物的感光细胞内节均有Mn-SOD的存在。在诱导光暴露的不同时间制备大鼠视网膜总RNA。使用GSH-PX cDNA探针进行Northern blot分析。采用抗GSH-PO抗体免疫组化法检测GSH-PO蛋白表达。早在光照后3小时，观察到神经视网膜中GSH-PO mRNA水平升高（对照组的100-145%）。然而，在其他时间点导致mRNA编码水平下降。第1天在感光细胞内节段发现GSH-PX免疫反应性，其他时间点未见。各时间点神经节细胞均出现GSH-PX免疫反应性。组织学上，光暴露组与对照组外核层萎缩无显著差异。这些结果提示，在组织中，Mn-SOD和GSH-PX可能参与了光暴露损伤的病理生理机制。

Manganese superoxide dismutase (Mn-SOD) is a naturally occurring scavenger of reactive oxygen intermediates. We hypothesized that Mn-SOD expression may be enhanced as a defensive mechanism against oxidative challenges, the intense light exposure. We examined the possibility that Mn-SOD expression is increased following light-induced damage of the retina. Rats were exposed to cyclic light (80 lux) for 2 weeks, and an intense light challenge (1800 lux) for 24 hours, and then returned to cyclic light. Eyes from these and control rats were obtained to 14 days after the light challenge, and protein expression was examined immunohistochemically using rabbit antisera against rat Mn-SOD.There was no significant difference between a light-exposed and a control groups with atrophy of the outer nuclear layrs. Mn-SOD were found in the photoreceptor inner segments on days 1,7 and 14 after light challenge in experimental animals.Total retinal RNA was prepared from rat at different times during the induction of light exposure. Northern blot analysis was performed using a GSH-PX cDNA probe. Protein expression of GSH-PO was examined by immunohistochemical method using anti-GSH-PO antibody. The mRNA levels for GSH-PO in the neural retina were observed to be increased (100-145% of controls) as early as 3 hours after light exposure. however, resulted in a decrease in the levels of mRNA coding with other time points. GSH-PX immunoreactivity was found in photoreceptor inner segments on day 1, but not detected other time points. GSH-PX immunoreactivity appeared in ganglion cells at all time points. Histologically, there was no significant difference between a light-exposed and a control groups with atrophy of the outer nuclear layrs. These results suggest that in tissue, Mn-SOD and GSH-PX may be responsible for the pathophysiology of light exposure injury.