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。我们推测，Mn-SOD的表达可能是作为一种防御氧化挑战的机制，即强光暴露。我们研究了在光诱导的视网膜损伤后，Mn-SOD表达增加的可能性。大鼠暴露于周期光(80勒克斯)2周，强光激发(1800勒克斯)24小时，然后返回到周期光。光照后至14d取眼，用兔抗大鼠锰超氧化物歧化酶抗血清进行免疫组织化学染色，观察外核层萎缩情况，光照组与对照组差异无统计学意义。实验动物在光照后1、7、14d的感光细胞内段均可检测到Mn-SOD的存在。用GSH-Px cDNA探针进行Northern印迹分析。用抗GSH-PO抗体免疫组织化学方法检测GSH-PO蛋白表达。GSH-PO在神经视网膜中的表达水平在光照后3小时即开始升高(为对照组的100-145%)。然而，与其他时间点相比，这导致了编码水平的下降。GSH-Px免疫反应在第1天出现在感光细胞内段，而在其他时间点未检测到。各时间点神经节细胞内均可见GSH-Px免疫反应阳性。光照组和对照组外核层萎缩在组织学上没有显著差异。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过程。

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.