当使用了过量药物或者药物发生严重的副作用时，快速的解毒剂就成为拯救病人的关键。这在抗凝血药物上尤其明显，抗凝血药物主要用于心脏病人的血栓治疗。但是当这种药物使用过量时，会造成致命的大出血。
??肝磷脂是一种抗凝剂，并且有特定的抑制药物。这种抗凝剂被广泛的使用，尽管有很多更好的抗凝剂不断被发明出来。德国波恩的一组科学家Alexander Heckel，Gunter Mayer，以及Bernd Potzsch最近发明了一种自身就携带了反抗凝因子的抗凝剂。当受到紫外线辐射时，这些分子的反抗凝因子就会被激发，使它们立即停止抗凝血作用。
??这种物质基于一种能和凝血酶结合的核酸（aptamer），凝血酶是一种在凝血过程中非常重要的蛋白质。Aptamer是DNA单链分子，能和其它分子——如凝血酶——结合。在小组实验中，aptamer折叠成三维结构，能和目标分子精密结合。科学家们将另一小段DNA结合在凝血酶aptamer上，这个小片段被激活后可以变为反抗凝因子。而只要它不被激活，分子就是一种很好的凝血剂。
??当aptamer的凝血作用需要被停止时，科学家就用紫外线激发小片段。这一小段DNA分子和结合凝血酶的aptamer是配对的，但是当一个小的核苷酸改变时，DNA链的彼此结合成双链分子的特性就会被阻止。
??紫外线能将这些变化的核苷酸分离出去，所以这些小片段就可以和aptamer结合。之前aptamer的三维结构被改变，同时变化的还有和凝血酶结合特性以及抗凝血作用。
英文原文：
Powerful drug comes with an 'off switch'
A new drug, designed with its own built-in antidote, could revolutionise drug safety, allowing effective use of potentially risky drugs.
Researchers have designed an anti-clotting drug that becomes inactive – allowing blood to form clots – when light of a specific frequency is shone on it.
Anti-clotting drugs are widely used in medicine, including in situations where the blood is transported outside of the body for a time, such as during heart surgery or kidney dialysis. But once back in the body, blood that cannot clot can cause catastrophic bleeding and stroke.
Heparin is often used as an anti-clotting agent in such situations, as it has an antidote that can be applied quickly if it is needed. But heparin can cause allergic reactions. Better, more modern anti-clotting agents cannot be used in these situations, however, as they have no fast antidote.
Shine a light
Alexander Heckel and colleagues at the University of Bonn, in Germany, may now have solved the problem. They have been experimenting with a “toolbox” of artificial nucleotides that change shape when bathed in light of a certain wavelength.
The team experimented with a potential anti-clotting drug called an aptamer, which is a string of 15 nucleotides – the building blocks of DNA. This aptamer works by binding and blocking a major molecule involved in the body’s blood-clotting reaction, called thrombin.
The researchers turned off this blocking action by causing the molecule to bend into a hairpin shape. They achieved this by stringing four extra nucleotides on one end of the aptamer. One of these was a shape-changing nucleotide, while the others were nucleotides that would normally bind with the sequence of nucleotides at the other end of the aptamer.
Without the right kind of light, the shape-changing nucleotide did not match its opposite number at the other end of the aptamer, and the two ends did not bind together. But when the light was switched on, the artificial nucleotide changed shape and became a match. This allowed the two ends of the aptamer to bind together in the hairpin shape, switching off the aptamer's anti-clotting action.
The team found it could "turn off" the aptamer in seconds, even when it was already bound to thrombin.
Such light-sensitive artificial nucleotides might be added to other nucleotide-based drugs, the researchers say. This could include drugs to control gene regulation and many crucial proteins.
