呋喃西林及其硝基自由对DNA的损伤的电化学研究【精品-doc】

呋喃西林及其硝基自由对DNA的损伤的电化学研究【精品-doc】 呋喃西林及其硝基自由对DNA的损伤的电化学研究 *王苹苹～倪永年 *南昌大学化学系，南昌，330031 *E-mail: ynni@ncu.edu.cn 本文利用循环伏安法和微分脉冲伏安法研究了呋喃西林的电化学行为。在质子溶液(30%乙醇+70% Britton-Robinson缓冲溶液)中，随着pH值的增加，呋喃西林由一个还原峰分裂为两个还原峰，其实质是发生了歧化反应。两个生成的还原峰分别为硝基自由基的产生和硝基自由基进一步还原为羟氨基的两个过程。同时利用微分脉冲伏安法研究了呋喃西林与双链DNA在溶液中的反应，发现产生自由基的还原峰并没有发生变化，而另一还原峰发生了峰电流下降峰电位负移的现象，硝基自由在呋喃西林与DNA反应的过程 3+起主导作用。本文还利用电化学探针Co(phen)和DNA生物传感器实现了呋喃西林对DNA损伤的间接检测。3 此外，利用构建的DNA生物传感器对还原前后呋喃西林对DNA损伤的进行了比较，发现连续在0到-0.9V的范围内对呋喃西林进行阴极扫描10圈(即不断还原呋喃西林)后，监测到的DNA鸟嘌呤和腺嘌呤的特征氧化峰明显大于不被还原时的响应，说明硝基自由基能够造成DNA的氧化损伤并远大于对呋喃西林本身。并与不进行阴极扫描即不对呋喃西林还原时的情况进行比较。以上实验说明，在体内代谢过程中，呋喃西林不仅本身对人体造成有危害，其代谢中间产物硝基自由基也会导致DNA的直接损伤，并占主导地位。 3+关键词:伏安法;DNA损伤;Co(phen);呋喃西林;硝基自由基 3 参考文献 [1] Zhang, W., Yang, T., Li, W., Li, G., Jiao, K. Biosens. Bioelectron. 2010, 25(10): 2370. [2] Arvand, M., Ansari R., Heydari. L. Mater. Sci. Eng., C. 2011, 31(8): 1819. [3] Wang, Y., Ni, Y., Kokot, S. Anal. Biochem. 2011, 419(2): 76. Voltammetric Detection of DNA Damage Induced by Nitrofurazone and Short-lived Nitro Radicals Using an Electrochemical DNA Biosensor Pingping Wang,Yongnian Ni* Department of Chemistry, Nanchang University, Nanchang 330031, China The electrochemical mechanism of nitrofurazone (NFZ) was investigated by the methods of cyclic voltammetry (CV) and differential pulse voltammetry (DPV). The pH-dependent behavior of nitrofurazone (NFZ) was studied at a glass carbon electrode in the protic medium (ethanol/Britton-Robinson buffer (30:70)). It was found that 23+short-lived nitro radicals could be generated by the disproportionation reaction of NFZ in the protic medium with high pH (larger than 7). In the presence of DNA, the DPV peak current of NFZ was decreased and the peak potential negatively shifted, indicating that there is an electrostatic interaction between NFZ and DNA. An electrochemical DNA biosensor was prepared to study the DNA damages. It was found that NFZ can lead to the damage of DNA by forming the N-deoxyguanine adducts, when Co(phen) was used as an electroactive probe. Moreover, the occurrence of the oxidation peaks of guanosine (750 mV) and adenosine (980 mV) indicated the 3DNA damage could be caused directly by short-lived nitro radicals, which were generated by reduction of the NFZ. All these experiments demonstrated that DNA damage would be happened with two different procedures, while NFZ was metabolized, and the nitro radicals were considered to be mainly responsible for the carcinogenic activity of NFZ in vivo.