金属离子对噻嗪酮与小牛胸腺DNA相互作用的影响

为探讨噻嗪酮及金属离子共存对非靶标生物遗传毒性的机制,利用紫外、荧光光谱法研究生理条件下噻嗪酮与小牛胸腺DNA(ctDNA)之间的结合作用大小及模式,从分子水平上分析了Cd~(2+)、Co~(2+)、Cu~(2+)、Ni~(2+)存在时对噻嗪酮与ctDNA相互作用的影响。结果表明:噻嗪酮可与ctDNA结合引起噻嗪酮吸收光谱明显红移;可与亚甲基蓝(MB)竞争结合ctDNA,且结合常数K随温度升高呈递减趋势;可与ctDNA以嵌插方式结合使熔点明显升高。环境金属离子的存在不会改变噻嗪酮与ctDNA之间的作用模式,但会影响其结合强弱,低浓度Cu~(2+)、Ni~(2+)可通过离子桥表现出一定的促结合作用,高浓度时则引起DNA结构改变而削弱噻嗪酮与DNA的结合,Co~(2+)、Cd~(2+)能影响DNA分子结构、与噻嗪酮竞争结合位点,导致结合常数下降。

Interaction properties of buprofezin to calf thymus DNA in the presence of metal ions

To illustrate the genetic toxicity mechanism of thiadiazine pesticides on non-target organisms, the interaction between buprofezin and calf thymus DNA(ctDNA) in vitro was investigated by UV-vis absorption spectroscopy and fluorescent spectrometry. The influences of heavy metals(Cd²⁺, Co²⁺, Cu²⁺ and Ni²⁺) on the binding properties were also studied at the molecular level, using methylene blue(MB) as a probe of DNA. The results showed that there was a distinct red shift of absorption spectrum by addition of ctDNA which can be ascribed to the binding interaction between buprofezin and ctDNA. Fluorescent experiments indicated that buprofezin was bound to ctDNA in competition with MB, and the binding constants decreased as a function of temperature. Furthermore, DNA melting-point increment suggested that the binding of buprofezin to ctDNA was an intercalative mode. The presence of metal ions did not change the interaction mode between buprofezin and ctDNA, but influenced the binding intensity of buprofezin to ctDNA. A small quantity of Cu²⁺ and Ni²⁺ showed a promotion between buprofezin and ctDNA via an ionic-bridge mechanism, but a large quantity of ions would modify the structure of ctDNA and weaken the binding capacity. Meanwhile, Co²⁺ and Cd²⁺ could penetrate the ctDNA and competitively bind to ctDNA, resulting in the declination of binding constant.