Condorelli G, Constanzo L L, De Guidi G, Giuffrida S, Sortino S
Dipartimento di Scienze Chimiche, Università di Catania, Italy.
Photochem Photobiol. 1995 Jul;62(1):155-61. doi: 10.1111/j.1751-1097.1995.tb05252.x.
Ultraviolet-A irradiation of a suprofen (2-[4-2(2-thenoyl) phenyl]propionic acid) (SPF) buffered solution (pH 7.4) in the presence of supercoiled pBR322 DNA leads to single strand breaks with the formation of an open circular form and subsequent linearization of the plasmid. On the basis of agarose gel electrophoresis data of samples irradiated in an air-saturated solution or in an oxygen-modified atmosphere, and the effects of sodium azide, D20, mannitol, copper(II), superoxide dismutase, 2-H-propanol, deferoxamine and surfactants, we suggest a photosensitization mechanism involving singlet oxygen and free radicals. The higher rate of photocleavage in nitrogen compared to that in an air-saturated solution and the results obtained from oxygen consumption measurements support the hypothesis that both the type I and type II photosensitization mechanisms are operative and that oxygen quenches the excited state of the irradiated drug. The photosensitization model applied was in agreement with that previously applied to cell membrane SPF photoinduced damage. Interaction of the drug with DNA, studied through circular dichroism and fluorescence anisotropy, probably occurs through a surface binding mode. The experimental techniques used for assessing the photodamaging activity of this drug may be useful for screening of phototoxic compounds in the environment and for determining the active species involved.
在超螺旋pBR322 DNA存在的情况下，对舒洛芬（2-[4-2(2-噻吩甲酰基)苯基]丙酸）（SPF）缓冲溶液（pH 7.4）进行紫外线A照射，会导致单链断裂，形成开环形式并随后使质粒线性化。根据在空气饱和溶液或氧改性气氛中照射的样品的琼脂糖凝胶电泳数据，以及叠氮化钠、D2O、甘露醇、铜（II）、超氧化物歧化酶、2-丙醇、去铁胺和表面活性剂的影响，我们提出了一种涉及单线态氧和自由基的光敏化机制。与空气饱和溶液相比，氮气中光裂解速率更高，以及耗氧量测量结果支持以下假设：I型和II型光敏化机制均起作用，并且氧淬灭了被照射药物的激发态。所应用的光敏化模型与先前应用于细胞膜SPF光诱导损伤的模型一致。通过圆二色性和荧光各向异性研究的药物与DNA的相互作用，可能通过表面结合模式发生。用于评估该药物光损伤活性的实验技术，可能有助于筛选环境中的光毒性化合物以及确定其中涉及的活性物种。
