核酸:与太阳紫外线辐射的相互作用。

T M Murphy
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引用次数: 0

摘要

减少平流层臭氧量的大气污染物可能显著增加到达地球表面的中波长太阳紫外线辐射的通量。与短波长的杀菌紫外线辐射(小于280 nm)一样,这些中间波长的紫外线(280-315 nm)可以促进核酸中的光化学反应,导致诸如环丁二嘧啶和单链和双链断裂等产物的出现。这些光化学反应强烈地影响着核酸的生物活性。计算机技术现在可用于预测纯化核酸体外辐照增加的化学和生物效应。然而,由于细胞中增敏剂的存在和核酸修复过程的作用,体内紫外线照射增加的效果变得复杂。有强有力的证据表明,对核酸的体内损伤会损伤受辐照的细胞和组织,但需要进一步的研究来定量预测太阳紫外线增加的生理后果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nucleic acids: interaction with solar UV radiation.

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.

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