Abstract
AbstractCisplatin is cis-diamminedichloroplatinum (II) of chemical formula, Pt(NH3)Cl2, abbreviated as cis-DDP and known commercially as platinol. It is used widely as an anticancer drug for various types of cancer, ever since its discovery two centuries ago and has become a target of extensive researches. Transplatin, trans-DDP on the other hand, is found to be less or ineffective to treat cancers. Cisplatin is known to interact mainly with the N(7) nitrogen of guanine in nucleic acids, after a water molecule takes away one of the chlorines by hydrolysis. This initiates the damage of nucleic acids and eventually leads to apoptosis. However the way how this happens and why transplatin is less effective is not completely clear. Here the author brings some new insights, using the precise structures of these molecules at the atomic level, how cisplatin can interact with the nitrogen of guanine and adenine and rupture the hydrogen bonding in the Watson Crick base pairs and damage the structure of DNA. It is hoped that the results presented here will contribute to a better atomistic insight into the structure, bonding and feasibility of the biochemical reactions involving these compounds and their derivates for the alleviation of cancer.
Highlights
The action of cisplatin as an anticancer agent is attributed to its binding mainly with the N(7) of guanine[1,2,3,4,5] which is one of the two purines forming the Watson Crick base pairs
While the first chlorine binds to guanine, the second chlorine of cis-DDP can removed by another water molecule and the guanine-Pt(NH3)[2] complex binds to a second available nitrogen of a nearby base pair
Cisplatin is known to interact mainly with the Nd.b.(7) of guanine, other reactive nitrogens in the Watson -Crick base pairs like Nd.b.(3) of adenine are vulnerable
Summary
The action of cisplatin as an anticancer agent is attributed to its binding mainly with the N(7) of guanine[1,2,3,4,5] which is one of the two purines forming the Watson Crick base pairs.
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