Department of Zoology, Faculty of Science, Mansoura University, Mansoura, Egypt.
Clin Exp Ophthalmol. 2014 Mar;42(2):169-81. doi: 10.1111/ceo.12123. Epub 2013 May 22.
Aging is a biological phenomenon that involves an increase of oxidative stress associated with gradual degradation of the structure and function of the retina. Gender differences and subsequent deterioration of retinal cell layers is an interesting topic, especially because there is no published work concerning it.
One hundred and twenty male and female Wistar albino rats ages 1, 6, 18, 30 and 42 months (n = 20 equal for male and female) were used. At the time interval, retinae were investigated by light and transmission electron microscopy, assessments of neurotransmitters, anti-oxidant enzymes (catalase, superoxide dismustase and glutathione S transferase), caspase-3 and -7, malonadialdhyde, and DNA fragmentation.
Light and transmission electron microscopy observations of the older specimens (30 and 42 months) revealed apparent deterioration of retinal cell layers, especially ganglion and nerve fibres, nuclear, pigmented epithelium and stacked membranes of the photoreceptor's outer segments. Males were highly susceptible to aging processes. Retinal DNA fragmentation was remarked parallel with increase of apoptic markers caspase 3 and 7. Concomitantly, there was a marked reduction of neurotransmitters and anti-oxidant enzymes, and an increase of lipid peroxidation.
Aging contributed to an increase of oxidative stress resulting from damage of mitochondria in retinal cells, a decrease of the anti-oxidant enzyme system and an increase of markers of retinal cell death.
衰老是一种生物现象,涉及与视网膜结构和功能逐渐退化相关的氧化应激增加。性别差异以及随后的视网膜细胞层恶化是一个有趣的话题,特别是因为没有关于它的已发表的工作。
120 只雄性和雌性 Wistar 白化大鼠,年龄分别为 1、6、18、30 和 42 个月(n = 20 只雄性和雌性各 20 只)。在时间间隔内,用光镜和透射电镜研究视网膜,评估神经递质、抗氧化酶(过氧化氢酶、超氧化物歧化酶和谷胱甘肽 S 转移酶)、半胱天冬酶-3 和 -7、丙二醛和 DNA 片段。
较老标本(30 和 42 个月)的光镜和透射电镜观察显示,视网膜细胞层,特别是神经节和神经纤维、核、色素上皮和光感受器外段堆叠膜明显恶化。雄性对衰老过程高度敏感。视网膜 DNA 片段与凋亡标志物 caspase 3 和 7 的增加平行出现。同时,神经递质和抗氧化酶显著减少,脂质过氧化增加。
衰老导致氧化应激增加,这是由于视网膜细胞中线粒体损伤、抗氧化酶系统减少和视网膜细胞死亡标志物增加所致。