Murphy T M
Curr Top Radiat Res Q. 1975 Jun;10(3):199-228.
Atmospheric pollutants that reduce the amount of ozone in the stratosphere may markedly increase the flux of intermediate-wavelength solar ultraviolet (UV) radiation that reaches the Earth's surface. Like short-wavelength germicidal UV radiation (less than 280 nm), these intermediate UV wavelengths (280-315 nm) can promote photochemical reactions in nucleic acids, leading to the appearance of such products as cyclobutadipyrimidines and single- and double-strand breaks. These photochemical reactions strongly affect the biological activities of the nucleic acids. Computer techniques are now available for predicting the chemical and biological effects of increased in vitro irradiation of purified nucleic acids. However, the effect of increased UV irradiation in vivo is complicated by the presence of sensitizing agents in cells and by the action of nucleic acid repair processes. There is strong evidence that in vivo damage to nucleic acids injures irradiated cells and tissues, but further research is needed to predict quantitatively the physiological consequences of increases in solar UV.
平流层中减少臭氧量的大气污染物可能会显著增加到达地球表面的中波太阳紫外线(UV)辐射通量。与短波杀菌紫外线辐射(小于280纳米)一样,这些中波紫外线波长(280 - 315纳米)可促进核酸中的光化学反应,导致诸如环丁烷二嘧啶以及单链和双链断裂等产物的出现。这些光化学反应强烈影响核酸的生物活性。现在已有计算机技术可用于预测纯化核酸体外照射增加所产生的化学和生物学效应。然而,体内紫外线照射增加的影响因细胞中敏化剂的存在以及核酸修复过程的作用而变得复杂。有强有力的证据表明,体内核酸损伤会损害受照射的细胞和组织,但需要进一步研究以定量预测太阳紫外线增加的生理后果。