ARTICLE pubs.acs.org/JPCA
Low-Energy Electron-Induced Single Strand Breaks in 20-Deoxycytidine-30 -monophosphate Using the Local Complex Potential Based Time-Dependent Wave Packet Approach Renjith B,† Somnath Bhowmick,† Manoj K. Mishra,‡ and Manabendra Sarma*,† † ‡
Department of Chemistry, Indian Institute of Technology Guwahati, Guwahati 781 039, India Department of Chemistry, Indian Institute of Technology Bombay, Powai, Mumbai 400 076, India
bS Supporting Information ABSTRACT: Recent experimental and theoretical investigations on resonant electron scattering off DNA and DNA fragments using low-energy electrons (LEEs), to propose the mechanism for single strand breaks (SSBs) and double strand breaks (DSBs), have received considerable attention. It is our purpose here to understand theoretically the comprehensive route to SSB in a selected DNA fragment, namely, 20 -deoxycytidine-30 -monophosphate (30 -dCMPH), induced by LEE (03 eV) scattering using the local complex potential based time-dependent wave packet (LCP-TDWP) approach. To the best of our knowledge, there is no time-dependent quantum mechanical study that has been reported in the literature for this DNA fragment to date. Initial results obtained from our calculation in the gas phase provide a good agreement with experimental observation and show the plausibility of SSB at 0.75 eV, which is very close to the highest SSB yield reported from the experimental measurement (0.8 eV) on plasmid DNA in the condensed phase.
’ INTRODUCTION Irradiation with ionizing radiation like β, γ, UV, X-rays, and so forth on living cells produces secondary electrons in abundance within the kinetic energy range of 120 eV.18 These secondary electrons, once generated inside the cell, gradually loose energy through inelastic collisions with other biomolecules and eventually become solvated within 1 ps.9 During the course of electron formation to solvation, they are highly active enough to ionize biomolecules like DNA and create potentially lethal lesions to such systems.6,10 It has recently been found that low-energy (03 eV) electrons (LEEs) can also induce DNA/RNA lesions like strand breaking, alteration to bases, sugar destruction, cross-link and dimer formation and so forth935 due to the formation of compound anionic metastable states in DNA oligomers, DNA bases, and uracil.20,27,36 Clustered DNA damages,6 mostly mutagenic in nature, eventually lead to the pathogenesis of cancer,14 apoptosis, and many other aging-related diseases.2 Therefore, the study of how LEEs induce DNA lesions like single strand breaks (SSBs), double strand breaks (DSBs), multiple double strand breaks (MDSBs), and so forth has become a prominent area of research both experimentally and theoretically in recent times.10,12,13,1622,2535 At the outset, these studies not only help to unfold the chemical formulations behind DNA damage but also open up a new avenue for understanding the biological effects of low-energy radiation and provide immense applications for the improvement of r 2011 American Chemical Society
radiation therapy.30,31 At the same time, incidents like nuclear explosion and, more recently, the cataclysm that took place at Fukushima (Japan) impose the risk factor of cancer from radioactive radiation. Hence, the current technology employed for cancer treatment has to be well equipped to minimize the after effect from such radiation. In a way, we can visualize electron-induced DNA damage as an electronmolecule scattering phenomenon. The work in this area started experimentally by Bouda€iffa et al., and their results signified the involvement of core-excited resonance through which DNA lesions were triggered.10 However, as suggested by Aflatooni et al.,36 Barrios et al. investigated SSB in a selected DNA fragment known as 20 -deoxycytidine-30 -monophosphate (30 -dCMPH) to find the role of shape resonance using very LEEs (below 3 eV) and inferred the possibility of SSB in the solvent medium19 and later on in the gas phase by Gu et al. for the same system.26 Along the same line, Illenberger and M€ark groups considered many possible DNA components for damage and identified that all of the DNA bases can attach LEE. In all cases, their findings were pointing toward the involvement of shape resonance phenomenon during DNA damage.14,15 In general, three sites were reported where DNA damage could be induced by LEEs,27 out of which, the DNA backbone, Received: August 18, 2011 Revised: October 12, 2011 Published: October 14, 2011 13753
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Figure 1. Fragment excised from a DNA molecule representing the basesugarphosphate group (taken from ref 19) in blue inside of the circle, while the bond susceptible to cleave is labeled with a red arrow.
that is, the sugarphosphate (CO) bond, is more susceptible to scission than the base NH and glycosidic (NC) bonds due to the lowest activation energy barrier for the electron to overcome during the CO bond cleavage. In addition, large electron affinity of the phosphate radical (∼5 eV)27,29 enforces electron migration to that site; such a phenomenon favors cleavage of the CO bond.19,21,22,27,29 Moreover, for the most favorable positions where the attachment of LEE was assumed to be either the baseπ* or phosphate PdO π* orbital, the former is preferred for LEE attachment in the 03 eV range.27,29 Many possible mechanisms were proposed for DNA damage by various experimental and theoretical groups.10,14,22,2528 However, the principal mechanism behind such adverse processes proceeds via the formation of a transient negative ion (TNI) followed by the dissociation of a covalent bond within the system, or in short what is known as dissociative electron attachment (DEA).12 Recently, we have developed a new implementation of the local complex potential based time-dependent wave packet (LCP-TDWP) approach for the calculation of vibrational excitation cross sections in electronmolecule scattering. The method has been applied to systems like resonant eN2, eH2, and eCO scattering, and results obtained are quite reasonable.37,38 A single calculation can provide the cross-section profile for a wide range of energy values. The necessary ingredients in our method are the target potential energy (PE) curve, the anionic PE curve, and the anionic decay function resulting from electron attachment. With the basic foundation from those works, we would like to canvas this new approach in a larger molecular network, that is, 30 -dCMPH in the present context, to investigate the characteristics of SSB via DEA in the low-energy regime (03 eV). Therefore, it is our purpose in this paper to understand how LEE induces SSB using time-dependent quantum mechanical perspectives and to provide a rigorous quantitative formalism rather than qualitative ones that were proposed by other groups.10,14,22,2528 An outline of computational considerations
is provided in the following section, and a discussion of prominent results is presented thereafter. A summary of the main observations concludes this paper.
’ METHOD It is difficult to consider in vivo DNA as a computational model for our study because of the presence of a large number of atoms, thereby making the system computationally expensive. In the case of real DNA, apart from a substantial amount of water being present, there are also counterions like Na+, K+, and so forth for neutralizing the negative charge on the phosphate group. Therefore, besides solvation, it is necessary to neutralize the negative charge on the phosphate group so that a reliable in vivo system can be approximated computationally. On the other hand, a gas-phase system, although not being identical to the solvated state, can be a suitable choice for exploring the mechanistic pathway of DNA damage. One such system that we have considered in this investigation as our system of interest is 30 -dCMPH (A) (Figure 1).19,26 The generated radical centers at the DNA backbone are neutralized by adding hydrogen, while the negative charge on the phosphate group is neutralized by adding a proton to ensure the smooth attachment of the incoming electron. The PE curves of neutral and anionic systems in the gas phase have been computed using the Gaussian 03 program suite.39 In this initial attempt, we have chosen the HartreeFock (HF) method and 6-31+G(d) as the basis set for calculating these PE curves. The neutral PE curve [EA(R)] has been generated from the optimized geometry stretching the labeled sugarphosphate CO bond at 256 equally discretized points in the interval of 110 a0 with a step size of 0.04 a0 using the rigid option. To calculate the anionic PE curve [EA(R)], we have added an electron to the LUMO π* orbital of the base and have utilized the unrestricted HF theory with the same basis set and options that we have used for the neutral molecule. 13754
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Further, electron attachment to the neutral molecule (A) leads to the formation of a metastable compound molecular anion (A), and the nuclear motion now evolves under the influence of the anionic Hamiltonian (HA). The nuclear motion of A in the time-dependent formalism can be written as37,38 ψi ðR, tÞ = eiHA ðRÞt=p ϕi ðRÞ
ð1Þ
with p2 2 ∇ þ WA ðRÞ HA ðRÞ ¼ 2μA
ð2Þ
and i WA ðRÞ ¼ EA ðRÞ ΓA ðRÞ 2
ð3Þ
where ψi(R,t) corresponds to the time evolution of the ith initial vibrational wave function ϕi(R) of the neutral target. μA and WA(R) are the reduced mass and local complex potential (LCP) of the metastable A, respectively. The vibrational eigen functions ϕi(R) and χi(R) are obtained by applying the Fourier grid Hamiltonian (FGH) method40 to EA(R) and EA(R) respectively. The FGH method has proved to be a versatile and efficient method for obtaining bound-state eigen values and eigen vectors. In the LCP formulation, the time evolution of the metastable anion is controlled by a complex energy, that is, ψn exp(iWnt/p) with Wn = En (i/2)Γn, where Wn is called LCP, as stated above. It follows that |ψn|2 exp(Γnt/p), and the real part of Wn, that is, En, serves as the PE of the anion in the time evolution of nuclear dynamics; the imaginary part Γn is related to the lifetime (τ) as τ = p/Γ and controls the decay pattern of the metastable anionic state. The nuclear motion of the metastable compound anion A therefore takes place in a complex potential,37,38,41,42 WA(R), whereby the availability of these complex potentials becomes the critical input to any investigation of the dynamical features underlying the formation and decay of these metastable resonances. The width function for the metastable anion ΓA(R) is calculated as a decaying exponential from our earlier investigations as37,38 ΓA ðRÞ ¼ δ1 expðαRÞ
∂ψi ^ A ψi ¼H ∂t
Finally, we have utilized the Fourier transform of the autocorrelation function Æχi(R)|ψi(R,t)æ, which is the projection of anionic eigen functions obtained using an anionic PE curve with a time-dependent wave function to calculate the fragmentation profile σ(E) as45 σðEÞ ¼
Z ∞ ∞
expðiEt=pÞÆχi ðRÞjψi ðR, tÞæ dt
ð6Þ
ð4Þ
where α is chosen such that ΓA(R) goes to zero at the crossing point R = Rx between EA(R) and EA(R), and δ1 has been chosen so that the wave function for nuclear motion exists only within the lifetime for a shape resonance phenomenon. We have used this model resonance width function from our earlier investigations on eN2, eH2, and eCO scattering37,38 due to the unavailability of the resonance width for the DNA fragment (Figure 1). As we can see from eq 4, one can control the decay pattern and consequently the nuclear motion of the wave function by controlling α and δ1. The time propagation is carried out by solving the timedependent Schr€odinger equation ip
Figure 2. (a) Potential energy curves for the neutral [EA(R)] and the real part [EA(R)] of the local complex potential [WA(R)] for A = 30 dCMPH, (b) the width function [ΓA(R)], and (c) ground-state vibrational eigenfunctions for neutral [ϕ0(R)] (solid line) and anionic [χ0(R)] (dashed line) systems.
ð5Þ
^ Aψi) of the The effect of the kinetic energy operator in (H anionic Hamiltonian on the initial vibrational wave function ψi(R,t=0) = ϕi(R) is effected by the fast Fourier transform technique,43 and the Lanczos scheme44 is used for time propagation of the initial wave function in our implementation.
’ RESULTS AND DISCUSSION As mentioned earlier, EA(R) and EA(R), where A = 30 dCMPH, have been calculated by stretching the labeled CO bond through 256 equally discretized points within the range of 110 a0 using the HF level of accuracy with 6-31+G(d) as the basis set and are plotted together in Figure 2a. From the PE curves (Figure 2a), it is seen that electron attachment is endothermic by ∼0.65 eV, whereas the electron affinity for the CO group calculated is ∼2.37 eV. The crossing point between neutral and anionic curves is at 5.04 a0 (2.66 Å). The width function, another ingredient, has been calculated using eq 4 at each grid points as a decaying function where the parameter δ1 is chosen to be 65 to sustain the metastability of the system and is shown in Figure 2b. The highest value of ΓA(R) = 103.8 eV is at the lowest CO bond length and may be due to the larger internuclear repulsion experienced by the two nuclei, whereas at equilibrium bond length, ΓA(R) has the value of 0.92 eV. Its value goes to zero at the crossing point and assists as a decaying function for the wave function in the nuclear dynamics. The vibrational eigenfunctions of neutral [ϕi(R)] and anionic [χi(R)] 13755
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Figure 3. Time evolution plots of the ground-state wave function ϕ0(R) (Figure 2c) under the effect of the anionic Hamiltonian at times t = 0, 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, and 22 fs.
systems have been calculated using the FGH method.40 In Figure 2c, we have plotted the ground-state vibrational wave functions of neutral and anionic systems. As we can see, both wave functions have similar spatial profiles as the neutral one, being slightly shifted toward the right turning point of the PE curve relative to the anionic wave function. The time evolution of the ground-state wave function of the neutral molecule under the effect of the metastable anionic Hamiltonian was initiated at time t = 0 and propagated in time steps of Δt = 1 au of time (∼0.02 fs) for a total of 8192 time steps (∼198 fs). Some snapshots of the time evolution at t = 0, 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, and 22 fs are presented in Figure 3. A careful analysis of the time evolution plots leads to the following remarks: (a) the amplitude of the wave function significantly diminishes with time, (b) the wave function moves slowly toward the right turning point of the classical region, (c) there is no reflection of the wave function from the right turning point, and (d) near 18 fs, the probability amplitude spreads over to the classical region. These observations from our nuclear dynamics calculation enable us to suggest that during the decay of the metastable anion, the CO bond does not get enough time to execute at least one vibration because, as mentioned by Barrios et al.,19 the vibrational period of a CO bond is around 33 fs. Notably, our calculation shows that the CO bond gets ruptured within 18 fs which falls under the expected shape resonance lifetime for this metastable species. Therefore, we support the mechanism provided by Gu et al.,26 where they discussed the possibility that electron migration from cytosine to sugarphosphate bond operates directly through the spatial overlap between atomic orbitals of the C6 of pyrimidine
Figure 4. Singly occupied molecular orbitals for the anionic 30 -dCMPH molecule at an equilibrium CO bond length of (a) 2.75 a0 (1.45 Å) where the extra electron is situated at the base π* orbital and (b) 5.67 a0 (3 Å) where the excess charge locates on the phosphate group.
and C30 of sugar, resembling an SN2-like mechanistic pathway. Therefore, the underlying phenomena during LEE-induced SSB may be outlined in following two steps. Step 1: LEE attachment to the LUMO of cytosine results in the formation of a metastable species. Step 2: The atomic orbital overlaps between the C6 center of the nonplanar cytosine and the C30 center of the sugar where the excess charge induces dissociation of the CO bond, tagged as “charge induced dissociation”, while migrating to the DNA backbone.26 The large electron affinity of the phosphate radical (∼5 eV)27,29 may favor the atomic orbital overlap and fission of the bond and thus generates a comparatively stable nucleoside radical as well as a phosphate anion. As suggested earlier, the time required for LEE-induced SSB from our calculation thus reinforces the above-mentioned steps because SN2 reactions are typically fast processes. Singly occupied molecular orbitals (SOMOs) of the anionic species (Figure 4) show that the electron migration from cytosine to the phosphate radical is evident as it resides in the base π* orbital at an equilibrium bond length (1.45 Å) (Figure 4a), while at larger bond length (3 Å) (Figure 4b), the electron is located on the phosphate radical. In Figure 5a, we have plotted the autocorrelation function (Æχ0(R)|ψ0(R,t)æ), which shows the maximum overlap when propagation starts and decreases exponentially to negligibly small 13756
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and so forth with different basis sets so that a comparative analysis can be made for the mechanistic pathway to SSB induced by LEE. In addition, we would like to examine the present fragment (Figure 1) for SSB in the solvent phase, and it is also our intent to observe the effects of electron-withdrawing and electron-donating groups within the same system. An effort along these lines is underway in our group.
’ ASSOCIATED CONTENT
bS
Supporting Information. Figures showing the singly occupied molecular orbital at 2.2 Å and comparison of the calculated fragmentation profile for different δ1 values with experimental result. This material is available free of charge via the Internet at http://pubs.acs.org.
’ AUTHOR INFORMATION Corresponding Author Figure 5. (a) Calculated autocorrelation function |Æχ0(R)|ψ0(R,t)æ| and (b) comparison of the corresponding fragmentation profile, σ(E), of (a) with experimental results.16
values at t = 10 fs. Fourier transformation of this autocorrelation function yields the fragmentation profile and is compared with that of experimental investigation on plasmid DNA in the condensed phase,16 shown in Figure 5b. As we can see from our fragmentation profile, the maximum peak position is found to be around 0.75 eV, which is in very good agreement with the experimental maximum peak position (0.8 eV) and assures the involvement of shape resonance phenomena during SSB. The structureless feature in the fragmentation profile may be linked to the impulse model42 classification, and this can be confirmed from time evolution plots of Figure 3, where only simple diminution of the probability amplitude with no typical movement of the amplitude between right and left turning points of the PE curve is seen. Therefore, our approach may provide new insight into the area of electron-induced scattering in DNA and its related fragments.
’ CONCLUDING REMARKS Our objective in this work is to offer a quantitative profile for low-energy electron-induced SSB in 30 -dCMPH using the local complex potential based time-dependent wave packet approach. Preliminary results from our calculations are shown to be in agreement with earlier investigations26 by highlighting the involvement of shape resonance phenomena through which SSB can occur in the gas phase for this fragment. Most of the earlier theoretical findings19,27,29 suggested that SSB can be activated only for a solvated system using LEEs. However, Gu et al. showed the presence of a low activation energy (6.2 kcal/mol) barrier during CO bond cleavage and proposed the possibility of SSB in the gas phase for the same moiety from their time-independent study.26 To the best of our knowledge, no theoretical cross section is available in the literature for this DNA fragment using time-dependent quantum mechanical treatment to date. Thus, our time-dependent study has provided a direct comparison between theoretical and experimental results for the first time. We hope our findings from LCP-TDWP calculations offer a starting point for further investigations on LEE-induced scattering in DNA and DNA fragments. We would like to generate the PE curves for this system using correlated methods like DFT, MP2,
*E-mail:
[email protected]. Fax: (+) 91 361 258 2349.
’ ACKNOWLEDGMENT This work has been supported by a grant from the Department of Science and Technology (DST) [Grant No. SR/FT/CS-029/ 2008], India, to M.S. R.B. acknowledges the financial support from the Ministry of Human Resource Development (MHRD), Government of India. S.B. is pleased to acknowledge DST for a fellowship. We are also grateful to IIT Guwahati for providing infrastructure facilities. ’ REFERENCES (1) von Sonntag, C. The Chemical Basis for Radiation Biology; Taylor and Francis: London, 1987. (2) Yamamoto, O.; Smith, K. Aging, Carcinogenesis and Radiation Biology; Plennum: New York, 1976; p 165. (3) Fuciarelli, A. F.; Zimbrick, J. D. Radiation Damage in DNA: Structure/Function Relationships at Early Times; Battelle: Columbus, OH, 1995. (4) Hagen, U.; Harder, D.; Jung, H.; Streffer, C. Radiation Research 18951995 Congress Proceedings, Vol. 2: Congress Lectures, 10th ICRR; Universit€atsdruckerei H. St€urtz AG, W€urburg, 1995. (5) LaVerne, J. A.; Pimblott, S. M. Radiat. Res. 1995, 141, 208–215. (6) Michael, B. D.; Neil, P. O’. Science 2000, 287, 1603–1604. (7) Swiderek, P. Angew. Chem., Int. Ed. 2006, 45, 4056–4059. (8) Pimblott, S. M.; LaVerne, J. A. Radiat. Phys. Chem. 2007, 76, 1244–1247. (9) Hanel, G.; Gstir, B.; Denfil, S.; Scheier, P.; Probst, M.; Farizon, B.; Farizon, M.; Illenberger, E.; Mark, T. D. Phys. Rev. Lett. 2003, 90, 1881041–1881044. (10) Bouda€iffa, B.; Cloutier, P.; Hunting, D.; Huels, M. A.; Sanche, L. Science 2000, 287, 1658–1660. (11) Huels, M. A.; Hahndorf., I.; Illenberger, E.; Sanche, L. J. Chem. Phys. 1998, 108, 1309–1312. (12) Huels, M. A.; Bouda€iffa, B.; Cloutier, P.; Hunting, D.; Sanche, L. J. Am. Chem. Soc. 2003, 125, 4467–4477. (13) Pan, X.; Cloutier, P.; Hunting, D.; Sanche, L. Phys. Rev. Lett. 2003, 90, 2081021–2081024. (14) Abdoul-Carime, H.; Gohlke, S.; Fischbach, E.; Scheinke, J.; Illenberger, E. Chem. Phys. Lett. 2004, 387, 267–270. (15) Ptasi nska, S.; Denfl, S.; Scheier, P.; Illenberger, E.; M€ark, T. D. Angew. Chem., Int. Ed. 2005, 44, 6941–6943. (16) Martin, F.; Burrow, P. D.; Cai, Z.; Cloutier, P.; Hunting, D.; Sanche, L. Phys. Rev. Lett. 2004, 93, 0681011–0681014. (17) Sanche, L. Eur. Phys. J. D 2005, 35, 367–390. 13757
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