Eaton J W
Division of Experimental Pathology, Albany Medical College, NY 12208, USA.
Doc Ophthalmol. 1994;88(3-4):233-42. doi: 10.1007/BF01203677.
A number of epidemiologic and experimental studies indirectly support the idea that solar ultraviolet radiation may be cataractogenic. However, the physical and cellular processes which might be involved in such cataractogenesis are by no means clear. Because a major consequence of the UV irradiation of oxygenated organic matter is the production of activated oxygen species, the involvement of oxidants has been suspected to be of importance. However, because the lens may normally exist in an hypoxic or even anoxic environment, the extent of availability of oxygen for such reactions is presently unknown. So also are the possible mechanism through which putative UV damage of the lens might eventuate in cataract. In addition to possible rapid and direct lethal damage to lens epithelium, possible cumulative damage to both lenticular DNA and proteins may occur. Furthermore, UV radiation has the potential to photolytically destroy light-sensitive nutrients and to generate damaging oxidants through interaction with ferruginous compounds. Given that Nature has probably provided the lens with substantial protective devices to ward off damaging effects of UV light, it is still an open question as to whether solar radiation contributes to cataract formation and, if so, by what mechanisms.
多项流行病学和实验研究间接支持了太阳紫外线辐射可能致白内障的观点。然而，这种白内障形成过程中可能涉及的物理和细胞过程尚不清楚。由于对含氧有机物进行紫外线照射的一个主要后果是产生活性氧，因此人们怀疑氧化剂的参与具有重要意义。然而，由于晶状体通常可能存在于低氧甚至无氧环境中，目前尚不清楚此类反应中氧气的可利用程度。晶状体可能的紫外线损伤最终导致白内障的可能机制也是如此。除了可能对晶状体上皮造成快速直接的致命损伤外，还可能对晶状体DNA和蛋白质造成累积损伤。此外，紫外线辐射有可能光解破坏光敏营养素，并通过与含铁化合物相互作用产生具有破坏性的氧化剂。鉴于大自然可能为晶状体提供了大量保护机制以抵御紫外线的破坏作用，太阳辐射是否会导致白内障形成，如果会，又是通过什么机制，仍然是一个悬而未决的问题。
