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多年来,阳光一直被疑为是参与人类白内障生成的因素。只是近10年才得到科学的支持。目前,已知长波或近紫外线光(300—400nm)可诱发晶体蛋白的化学变化以及生长活跃的上皮细胞的细胞病理变化而损害晶体。此范围波长的辐射在分子水平被认为能抑制多种细胞的生长,不是像短波紫外线那样直接损伤DNA,而是诱发具有抑制作用的光化产物(photoproducts)。光氧化反应也可通过改变晶体结构蛋白及酶蛋白的性质而干扰其功能。由于臭氧层的存在,波长小于300nm光线不能达到地球,角膜几乎能吸收所有波长小于300nm光线,在白内障的生成过程中,自然短波紫外线可能不是重要的因素。长波紫外线光容易穿通角膜(在人约50%),因此这个高水平的辐射能最能达到晶体,比其它眼组织更有效地被吸收。此光几乎全部被游离分散的小分子和蛋白的芳香族基所吸收。在此情况下,光化学激发的自由基过程,可使色氨酸和其它芳香族氨基酸转化为光化产物,集聚在老年人
For years, the sun has been suspected of being a contributing factor to the formation of cataracts in humans. It took only 10 years to get scientific support. At present, it is known that long-wave or near-ultraviolet light (300-400 nm) can damage the crystal by inducing chemical changes of the crystal protein and cytopathological changes of the growing active epithelial cells. Radiation at this range of wavelengths is thought to inhibit, at the molecular level, the growth of a variety of cells, rather than directly damaging the DNA as shortwave UV but inducing photoproducts that have an inhibitory effect. Photooxidation can also interfere with its function by altering the properties of crystal structure proteins and enzyme proteins. Due to the presence of the ozone layer, light with wavelengths less than 300 nm can not reach the Earth, and cornea can absorb almost all light with wavelengths less than 300 nm. Natural short-wave UV may not be an important factor in the formation of cataract. Long-wave ultraviolet light easily penetrates the cornea (about 50% of people), so this high level of radiation best reaches the lens and is absorbed more efficiently than other ocular tissues. Almost all of this light is absorbed by the free radicals of the small molecules and the aromatic groups of the protein. In this case, the photochemical excitation of the free radical process, can tryptophan and other aromatic amino acids into photochemical products, gathered in the elderly