Defense mechanism for retinal light damage.

视网膜光损伤的防御机制。

基本信息

批准号：
06671769
负责人：
OHIRA Akihiro
金额：
$ 1.41万
依托单位：
Nagasaki University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06671769/
关键词：
LIGHT DAMAGE REACTIVE OXYGEN INTERMEDIATES RETINA DEFENSE MECHANISM SUPEROXIDE DISMUTASE ANTIOXIDANTS ADULTT CELL LEUKEMIA DERIVED FACTOR GLUTATHIONE PEROXIDASE 網膜光障害 SOD グルタチオン・ペルオキシダーゼ網膜視細胞 Adult T cell leukemia clerived factor

项目摘要

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.

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 表达可能会增强，作为对抗氧化挑战（强光照射）的防御机制。我们研究了光诱导视网膜损伤后 Mn-SOD 表达增加的可能性。将大鼠暴露在循环光（80 勒克斯）下 2 周，并接受强光挑战（1800 勒克斯）24 小时，然后返回循环光。光刺激后 14 天，取出这些大鼠和对照大鼠的眼睛，并使用针对大鼠 Mn-SOD 的兔抗血清进行免疫组织化学检查蛋白质表达。光暴露组和对照组之间没有显着差异，外层萎缩。核层。实验动物光激发后第1,7和14天在光感受器内节中发现了Mn-SOD。在诱导光照射的不同时间制备大鼠视网膜总RNA。使用 GSH-PX cDNA 探针进行 Northern 印迹分析。使用抗GSH-PO抗体通过免疫组织化学方法检查GSH-PO的蛋白表达。早在光照后 3 小时，就观察到神经视网膜中 GSH-PO 的 mRNA 水平增加（对照的 100-145%）。然而，导致其他时间点 mRNA 编码水平下降。第一天在光感受器内节中发现 GSH-PX 免疫反应性，但在其他时间点未检测到。 GSH-PX 免疫反应性在所有时间点都出现在神经节细胞中。组织学上，光暴露组和对照组之间没有显着差异，外核层萎缩。这些结果表明，在组织中，Mn-SOD 和 GSH-PX 可能与光暴露损伤的病理生理学有关。