Department of Chemistry, Case Western Reserve University, Cleveland, Ohio 44106, USA.
J Phys Chem B. 2011 Mar 31;115(12):3263-70. doi: 10.1021/jp112018u. Epub 2011 Mar 8.
Patients treated with the immunosuppressant and anticancer drugs 6-thioguanine, azathioprine, or mercaptopurine can metabolize and incorporate them in DNA as 6-thioguanosine. The skin of these patients is sensitive to UVA radiation, and long-term treatment can result in extremely high incidence of sunlight-induced skin cancer. In this contribution the photophysics of 6-thioguanosine have been studied in aqueous buffer solution and in acetonitrile after excitation with UVA light to provide mechanistic insights about the origin of its phototoxicity. It is shown that most of the initial excited-state population in the S(2)(ππ*, L(a)) state decays by ultrafast intersystem crossing to the triplet manifold. A triplet quantum yield of 0.8 ± 0.2 is determined in aqueous buffer solution. A minor fraction of the S(2) population bifurcates on an ultrafast time scale to populate the S(1)(n(S)π*) state, which decays back to the ground state in tens of picoseconds. Quantum-chemical calculations that include solvent effects support the experimental results. The high triplet yield of 6-thioguanosine, which we argue can result in photosensitization of molecular oxygen and photooxidative DNA damage, is proposed to explain the high phototoxicity exhibited by these pro-drugs in patients upon sunlight exposure. Finally, the experimental and computational results for 6-thioguanosine are compared with those reported for the DNA/RNA guanine monomers.
接受免疫抑制剂和抗癌药物 6-硫代鸟嘌呤、巯嘌呤或硫唑嘌呤治疗的患者可以将其代谢并整合到 DNA 中作为 6-硫代鸟苷。这些患者的皮肤对 UVA 辐射敏感,长期治疗会导致极高的阳光诱导皮肤癌发病率。在本研究中,我们研究了 6-硫代鸟苷在水缓冲溶液和乙腈中的光物理性质,用 UVA 光激发后提供了其光毒性的起源的机制见解。结果表明,S(2)(ππ*, L(a))态的初始激发态大部分通过超快系间窜跃衰减到三重态。在水缓冲溶液中确定了 0.8±0.2 的三重态量子产率。S(2)态的一小部分在超快时间尺度上分叉,以填充 S(1)(n(S)π*)态,该态在数十皮秒内回到基态。包括溶剂效应在内的量子化学计算支持实验结果。我们认为,6-硫代鸟苷的高三重态产率可能导致分子氧的光致敏和光氧化 DNA 损伤,这可以解释这些前药在阳光照射下患者表现出的高光毒性。最后,比较了 6-硫代鸟苷的实验和计算结果与 DNA/RNA 鸟嘌呤单体的结果。