Effect of cisplatin binding on guanine in nucleic acid: An ab initio studyстатья

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[1] Zilberberg I. L., Avdeev V. I., Zhidomirov G. M. Effect of cisplatin binding on guanine in nucleic acid: An ab initio study // Journal of Molecular Structure. — 1997. — Vol. 418, no. 1. — P. 73–81. To investigate the molecular mechanism of the antitumour activity of cisplatin, ab initio Hartree-Fock pseudo potential calculations have been performed for some Pt(II) complexes with the guanine nucleic base. We propose that cisplatin binding to guanine in DNA leads to a point mutation as the latter is the only change that the nucleic acid could "remember" after replication. Two ways of producing the point mutation are examined. The first is shifting the keto-enol tautomerization of guanine towards the enol form (rare in DNA) in the presence of cisplatin. The second is the action of cisplatin on the guanine-cytosine pairing in DNA through binding to the O6 site of guanine which is involved in one of three hydrogen bonds between these nucleic bases. For this purpose the complex of cis-Pt(NH3)2+3 and the hydrogen-bonded formamide-formamide pair has been calculated. The results obtained suggest, first, that the keto-enol tautomerization is not subject to crucial change in the presence of cisplatin. Second, it is found that the oxygen of the formamide coordinated by Pt(II) is no longer available for hydrogen bonding with the corresponding pan of the complementary molecule. Hence, one can predict that binding of cisplatin to the O6 site of guanine breaks the corresponding hydrogen bond between guanine and cytosine which, in turn, can cause the point mutation. © 1997 Elsevier Science B.V.

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