Rdination of metal leads to higher impact and hence the discrepancy in PO22 band shifting. It was observed that the band at 1694.4 cm21 (uC = O) for free DNA exhibited shifting at 1715 cm21 in DNA-Mg2+ complexes. The shifting in the vibrational stretching frequency of C = O in DNA-Mg2+ STA-9090 complexes is mainly attributed to the metal coordination with N7 guanine, N3 cytosine, thymine O2 and adenine N7. A similar kind of observation substantiates the above interaction [41,42]. Interestingly, in the presence of Mg2+, the C = O vibrational frequency of both drug and DNA disappeared and shifted to higher frequency at 1700, 1701, 1700.5 cm21 in Mg2+-DNA-theophylline, Mg2+-DNA-theobromine and Mg2+DNA-caffeine complexes correspondingly (Table 2) 18334597 (Fig. 6), indicating the enhanced binding of these drugs in the presence of Mg2+. The broadening of NH peak as observed as function of intramolecular H-bonding in free DNA (3600?900 cm21) (Fig. 4) was reduced in DNA-Mg2+ complexes (3550?000 cm21) (Fig. 6) (Table 2). The intramolecular H-bonding reduction by Mg2+ can be attributed to its coordination with DNA phosphates and also toN7 adenine/guanine, thymine O2 and N3 cytosine. The coordination effected by Mg2+ could be seen by comparing the vibrational stretching frequencies of C = O and PO22 bands in DNA-Mg2+ complexes. Intriguingly, the broadening effect was restored or reverted back to certain extant in Mg2+-DNAtheophylline (3600?950 cm21), Mg2+-DNA-theobromine (3550?2900 cm21) and Mg2+-DNA-caffeine (3500?100 cm21) complexes (Fig. 6) (Table 2), signifying that the reduced intramolecular Hbonding by Mg2+ favors the enhanced binding of methylxanthines with DNA through H-bonding interaction. In addition to the NH band, support for the enhanced binding of methylxanthines with DNA also comes from a) the changes in C = O vibrational frequency observed at 1715 cm21 of DNA-Mg2+ complexes b) shift in the bands of DNA bases (Ganetespib biological activity described below). The enhanced binding of methylxanthines with DNA in the vicinity of Mg2+ gains support due to shift in the bands of DNA bases or DNA in-plane vibrations in the region of 1707?1400 cm21 [41,42]. The band at 1707.3 cm21 (G, T) related to mainly guanine shifted to 1715, 1700, 1701 and 1700.5 in Mg2+DNA, Mg2+-DNA-theophylline, Mg2+-DNA-theobromine and Mg2+-DNA-caffeine complexes respectively. The changes observed in the band at 1658 cm21 (T, G, C) mainly for thymine [41,42], cytosine band at 1484.2 cm21 (C, G) and for adenine at 1600 cm21 upon drug complexation, indicating binding of methylxanthines were greatly enhanced in the presence of Mg2+. Especially theobromine binding was improved when compared to its non-metal complexes, where a minor change alone was noticed in the C = O frequency of drug (Fig. 3 and 4). Together with the changes observed in the PO22 band of DNA during complexation with metal and drugs, changes were also observed in the main IR marker bands at 890 cm21 (sugarphosphate stretch) and 836 (phosphodiester mode). These IR marker bands showed some variations in complexes at 897, 825 cm21 (Mg2+-DNA); 898 cm21 (Mg2+-DNA-theophylline); 895, 830 cm21 (Mg2+-DNA-theobromine) and 898, 832 cm21 (Mg2+-DNA-caffeine). Hence the DNA structure was shifted from B family to A- family in the above complexes. Other than the structural alteration, the changes in the PO22 band of DNA can also be attributed to the metal interaction with N7 adenine/ guanine, thymine O2 and N3 cytosine. Here the study encompassing the drug interact.Rdination of metal leads to higher impact and hence the discrepancy in PO22 band shifting. It was observed that the band at 1694.4 cm21 (uC = O) for free DNA exhibited shifting at 1715 cm21 in DNA-Mg2+ complexes. The shifting in the vibrational stretching frequency of C = O in DNA-Mg2+ complexes is mainly attributed to the metal coordination with N7 guanine, N3 cytosine, thymine O2 and adenine N7. A similar kind of observation substantiates the above interaction [41,42]. Interestingly, in the presence of Mg2+, the C = O vibrational frequency of both drug and DNA disappeared and shifted to higher frequency at 1700, 1701, 1700.5 cm21 in Mg2+-DNA-theophylline, Mg2+-DNA-theobromine and Mg2+DNA-caffeine complexes correspondingly (Table 2) 18334597 (Fig. 6), indicating the enhanced binding of these drugs in the presence of Mg2+. The broadening of NH peak as observed as function of intramolecular H-bonding in free DNA (3600?900 cm21) (Fig. 4) was reduced in DNA-Mg2+ complexes (3550?000 cm21) (Fig. 6) (Table 2). The intramolecular H-bonding reduction by Mg2+ can be attributed to its coordination with DNA phosphates and also toN7 adenine/guanine, thymine O2 and N3 cytosine. The coordination effected by Mg2+ could be seen by comparing the vibrational stretching frequencies of C = O and PO22 bands in DNA-Mg2+ complexes. Intriguingly, the broadening effect was restored or reverted back to certain extant in Mg2+-DNAtheophylline (3600?950 cm21), Mg2+-DNA-theobromine (3550?2900 cm21) and Mg2+-DNA-caffeine (3500?100 cm21) complexes (Fig. 6) (Table 2), signifying that the reduced intramolecular Hbonding by Mg2+ favors the enhanced binding of methylxanthines with DNA through H-bonding interaction. In addition to the NH band, support for the enhanced binding of methylxanthines with DNA also comes from a) the changes in C = O vibrational frequency observed at 1715 cm21 of DNA-Mg2+ complexes b) shift in the bands of DNA bases (described below). The enhanced binding of methylxanthines with DNA in the vicinity of Mg2+ gains support due to shift in the bands of DNA bases or DNA in-plane vibrations in the region of 1707?1400 cm21 [41,42]. The band at 1707.3 cm21 (G, T) related to mainly guanine shifted to 1715, 1700, 1701 and 1700.5 in Mg2+DNA, Mg2+-DNA-theophylline, Mg2+-DNA-theobromine and Mg2+-DNA-caffeine complexes respectively. The changes observed in the band at 1658 cm21 (T, G, C) mainly for thymine [41,42], cytosine band at 1484.2 cm21 (C, G) and for adenine at 1600 cm21 upon drug complexation, indicating binding of methylxanthines were greatly enhanced in the presence of Mg2+. Especially theobromine binding was improved when compared to its non-metal complexes, where a minor change alone was noticed in the C = O frequency of drug (Fig. 3 and 4). Together with the changes observed in the PO22 band of DNA during complexation with metal and drugs, changes were also observed in the main IR marker bands at 890 cm21 (sugarphosphate stretch) and 836 (phosphodiester mode). These IR marker bands showed some variations in complexes at 897, 825 cm21 (Mg2+-DNA); 898 cm21 (Mg2+-DNA-theophylline); 895, 830 cm21 (Mg2+-DNA-theobromine) and 898, 832 cm21 (Mg2+-DNA-caffeine). Hence the DNA structure was shifted from B family to A- family in the above complexes. Other than the structural alteration, the changes in the PO22 band of DNA can also be attributed to the metal interaction with N7 adenine/ guanine, thymine O2 and N3 cytosine. Here the study encompassing the drug interact.
