Čejková Jitka, Čejka Čestmír
Laboratory of Eye Histochemistry and Pharmacology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Histol Histopathol. 2015 Aug;30(8):893-900. doi: 10.14670/HH-11-611. Epub 2015 Mar 24.
In various corneal injuries (such as chemical burns or irradiation of corneas with UVB radiation) and ocular diseases (e.g. dry eye disease, keratokonus, bullous keratopathy, Fuchs' endothelial dystrophy), the expressions of malondialdehyde (a marker of lipid peroxidation) and nitrotyrosine (a marker of oxidative stress) appeared in cells of individual corneal layers and conjunctival cells (dry eye disease). This is in contrast to healthy corneas in which negligible levels of malondialdehyde and no expressions of nitrotyrosine are present. The injured or diseased corneas reveal decreased capacity of antioxidants (enzymatic as well as non-enzymatic), whereas the levels of pro-oxidants (e.g. oxidases that generate reactive oxygen species) remain at physiological levels or even increase, leading to the antioxidant/prooxidant imbalance and oxidative stress. Oxidative stress in the cornea stimulates generation of pro-inflammatory cytokines, proteolytic enzymes and enzymes that generate nitric oxide (nitric oxide synthases). An abundant amout of reactive oxygen species and nitric oxide lead to the formation of toxic reactive products contributing to tissue damage. This review aims to summarize immunohistochemical changes in severe corneal injuries and diseases in which oxidative stress has been proved.
在各种角膜损伤(如化学烧伤或用中波紫外线辐射角膜)和眼部疾病(如干眼症、圆锥角膜、大泡性角膜病变、富克斯内皮营养不良)中,丙二醛(脂质过氧化的标志物)和硝基酪氨酸(氧化应激的标志物)在角膜各层细胞和结膜细胞(干眼症)中均有表达。这与健康角膜形成对比,健康角膜中丙二醛水平可忽略不计且无硝基酪氨酸表达。受损或患病的角膜显示抗氧化剂(酶促和非酶促)能力下降,而促氧化剂(如产生活性氧的氧化酶)水平保持在生理水平甚至升高,导致抗氧化剂/促氧化剂失衡和氧化应激。角膜中的氧化应激刺激促炎细胞因子、蛋白水解酶和产一氧化氮的酶(一氧化氮合酶)的产生。大量的活性氧和一氧化氮导致形成有毒的反应产物,造成组织损伤。本综述旨在总结已证实存在氧化应激的严重角膜损伤和疾病中的免疫组织化学变化。