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表达可能是增强对氧化挑战，强光照射的防御机制。我们研究了Mn-SOD表达增加的可能性，以下光诱导的视网膜损伤。将大鼠暴露于周期性光（80 lux）2周，和强光激发（1800 lux）24小时，然后返回到周期性光。光刺激后14天取眼组织，用抗大鼠Mn-SOD的兔抗血清进行免疫组化检测，结果显示，光刺激组与对照组相比，外核层无明显萎缩。实验动物光刺激后第1、7、14天感光细胞内节均可见Mn-SOD的表达。用GSH-PX cDNA探针进行北方印迹分析。免疫组化法检测GSH-PO蛋白表达。早在光暴露后3小时，观察到神经视网膜中GSH-PO的mRNA水平增加（对照的100-145%）。然而，在其他时间点导致mRNA编码水平的降低。GSH-PX免疫反应在第1天的感光细胞内节，但没有检测到其他时间点。GSH-PX免疫反应出现在神经节细胞在所有时间点。组织学上，光暴露组和对照组的外核层萎缩无显著差异。提示组织中Mn-SOD和GSH-PX可能参与了光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.