Berthoud Viviana M, Beyer Eric C
Department of Pediatrics, University of Chicago, Chicago, Illinois 60637, USA.
Antioxid Redox Signal. 2009 Feb;11(2):339-53. doi: 10.1089/ars.2008.2119.
The eye lens is constantly subjected to oxidative stress from radiation and other sources. The lens has several mechanisms to protect its components from oxidative stress and to maintain its redox state, including enzymatic pathways and high concentrations of ascorbate and reduced glutathione. With aging, accumulation of oxidized lens components and decreased efficiency of repair mechanisms can contribute to the development of lens opacities or cataracts. Maintenance of transparency and homeostasis of the avascular lens depend on an extensive network of gap junctions. Communication through gap junction channels allows intercellular passage of molecules (up to 1 kDa) including antioxidants. Lens gap junctions and their constituent proteins, connexins (Cx43, Cx46, and Cx50), are also subject to the effects of oxidative stress. These observations suggest that oxidative stress-induced damage to connexins (and consequent altered intercellular communication) may contribute to cataract formation.
晶状体不断受到来自辐射及其他来源的氧化应激影响。晶状体有多种机制来保护其成分免受氧化应激并维持其氧化还原状态，包括酶促途径以及高浓度的抗坏血酸和还原型谷胱甘肽。随着年龄增长，晶状体氧化成分的积累以及修复机制效率的降低会促使晶状体混浊或白内障的形成。无血管晶状体的透明度和内环境稳态的维持依赖于广泛的缝隙连接网络。通过缝隙连接通道进行的通讯允许包括抗氧化剂在内的分子（分子量高达1 kDa）在细胞间通过。晶状体缝隙连接及其组成蛋白连接蛋白（Cx43、Cx46和Cx50）也会受到氧化应激的影响。这些观察结果表明，氧化应激诱导的连接蛋白损伤（以及随之改变的细胞间通讯）可能导致白内障的形成。
