Lipman R M, Tripathi B J, Tripathi R C
Department of Ophthalmology and Visual Science, University of Chicago, Illinois.
Surv Ophthalmol. 1988 Nov-Dec;33(3):200-10. doi: 10.1016/0039-6257(88)90088-4.
Microwaves most commonly cause anterior and/or posterior subcapsular lenticular opacities in experimental animals and, as shown in epidemiologic studies and case reports, in human subjects. The formation of cataracts seems to be related directly to the power of the microwave and the duration of exposure. The mechanism of cataractogenesis includes deformation of heat-labile enzymes, such as glutathione peroxide, that ordinarily protect lens cell proteins and membrane lipids from oxidative damage. Oxidation of protein sulfhydryl groups and the formation of high-molecular-weight aggregates cause local variations in the orderly structure of the lens cells. An alternative mechanism is thermoelastic expansion through which pressure waves in the aqueous humor cause direct physical damage to the lens cells. Cataracts induced by ionizing radiation (e.g., X-rays and gamma rays) usually are observed in the posterior region of the lens, often in the form of a posterior subcapsular cataract. Increasing the dose of ionizing radiation causes increasing opacification of the lens, which appears after a decreasing latency period. Like cataract formation by microwaves, cataractogenesis induced by ionizing radiation is associated with damage to the lens cell membrane. Another possible mechanism is damage to lens cell DNA, with decreases in the production of protective enzymes and in sulfur-sulfur bond formation, and with altered protein concentrations. Until further definitive conclusions about the mechanisms of microwaves and ionizing radiation induced cataracts are reached, and alternative protective measures are found, one can only recommend mechanical shielding from these radiations to minimize the possibility of development of radiation-induced cataracts.
在实验动物中,微波最常导致晶状体前囊下和/或后囊下混浊,并且如流行病学研究和病例报告所示,在人类受试者中也是如此。白内障的形成似乎与微波的功率和暴露持续时间直接相关。白内障形成的机制包括热不稳定酶(如谷胱甘肽过氧化物酶)的变形,这些酶通常可保护晶状体细胞蛋白质和膜脂质免受氧化损伤。蛋白质巯基的氧化和高分子量聚集体的形成会导致晶状体细胞有序结构的局部变化。另一种机制是热弹性膨胀,通过这种机制,房水中的压力波会对晶状体细胞造成直接的物理损伤。由电离辐射(如X射线和γ射线)引起的白内障通常在晶状体的后部区域观察到,通常以后囊下白内障的形式出现。增加电离辐射剂量会导致晶状体混浊加重,且潜伏期缩短后就会出现。与微波导致白内障形成一样,电离辐射引起的白内障形成也与晶状体细胞膜损伤有关。另一种可能的机制是晶状体细胞DNA受损,导致保护酶的产生减少、硫-硫键形成减少以及蛋白质浓度改变。在对微波和电离辐射诱发白内障的机制得出进一步明确结论并找到替代保护措施之前,人们只能建议对这些辐射进行机械屏蔽,以尽量减少辐射诱发白内障发生的可能性。