“…1,2 However mechanism of interactions between drug molecules and DNA is still relatively little known. It is necessary to introduce more simple methods for investigating the mechanism of interaction.…”
Neste trabalho, a interação de doxorrubicina com DNA (obtido de timo de bezerro) em fita dupla foi investigada através de técnicas de espectrofotometria UV-Vis, voltametria e espectrofluorometria, usando azul de metrileno (MB) como marcador. O comportamento voltamétrico da doxorrubicina foi investigado em eletrodo de carbono vítreo usando voltametria de pulso diferencial. A doxorrubicina é reduzida, produzindo um pico de redução. Os dois estudos, espectrofotometria UV-Vis e voltametria de pulso diferencial, confirmam a reação de intercalação. Os resultados mostraram que a doxorrubicina e a molécula de MB foram intercaladas na dupla hélice do DNA. A constante de ligação aparente de doxorrubicina com DNA foi 3,2 × 10 4 L mol -1 . O sinal de fluorescência da doxorrubicina e azul de metileno é suprimido com a adição de DNA. A equação de Stern-Volmer baseou-se na supressão do sinal de fluorescência da doxorrubicina.In this work, the interaction of doxorubicin with calf thymus double strand Deoxyribonucleic acid (ds-DNA) has been investigated with the use of Methylene Blue (MB) dye as a probe by the application of UV-Vis spectrophotometry, voltammetry and spectrofluorometry. The voltammetric behavior of doxorubicin has been investigated at glassy carbon electrode using differential pulse voltammetry. Doxorubicin is reduced, yielding one reduction peak. Both UV-Vis spectrophotometry and differential pulse voltammetry studies confirm the intercalation reaction. The results showed that both doxorubicin and the MB molecule could intercalate into the double helix of the DNA. The apparent binding constant of doxorubicin with DNA has been found to be 3.2 × 10 4 L mol -1 . The fluorescence signal of doxorubicin and methylene blue was quenched with DNA addition. The Stern-Volmer equation was plotted based on quenching fluorescence signal of doxorubicin.Keywords: doxorubicin, DNA, chemotherapy, spectrophotometry, voltammetry, spectrofluorometry
IntroductionStudy of interactions between drugs and DNA is very interesting and significant not only in understanding the mechanism of interaction, but also for the design of new drugs. 1,2 However mechanism of interactions between drug molecules and DNA is still relatively little known. It is necessary to introduce more simple methods for investigating the mechanism of interaction. By understanding the mechanism of interaction, designing of new DNA-targeted drugs and the screening of these in vitro will be possible.A great variety of substances, including several agents of importance in cancer chemotherapy, 3 are known to bind to DNA by intercalation. 4 Attention has been concentrated on the classical intercalating drugs, acridines and ethidium bromide. [4][5][6] Studies on the binding of various dyes, drugs and antibiotics to DNA and chromatin have contributed to the understanding of the structure of these macromolecules, 6-14 and have suggested possible mechanisms of the biological activity of some drugs. 3 Molecular models of the intercalation of some drugs into DNA have been describ...
“…1,2 However mechanism of interactions between drug molecules and DNA is still relatively little known. It is necessary to introduce more simple methods for investigating the mechanism of interaction.…”
Neste trabalho, a interação de doxorrubicina com DNA (obtido de timo de bezerro) em fita dupla foi investigada através de técnicas de espectrofotometria UV-Vis, voltametria e espectrofluorometria, usando azul de metrileno (MB) como marcador. O comportamento voltamétrico da doxorrubicina foi investigado em eletrodo de carbono vítreo usando voltametria de pulso diferencial. A doxorrubicina é reduzida, produzindo um pico de redução. Os dois estudos, espectrofotometria UV-Vis e voltametria de pulso diferencial, confirmam a reação de intercalação. Os resultados mostraram que a doxorrubicina e a molécula de MB foram intercaladas na dupla hélice do DNA. A constante de ligação aparente de doxorrubicina com DNA foi 3,2 × 10 4 L mol -1 . O sinal de fluorescência da doxorrubicina e azul de metileno é suprimido com a adição de DNA. A equação de Stern-Volmer baseou-se na supressão do sinal de fluorescência da doxorrubicina.In this work, the interaction of doxorubicin with calf thymus double strand Deoxyribonucleic acid (ds-DNA) has been investigated with the use of Methylene Blue (MB) dye as a probe by the application of UV-Vis spectrophotometry, voltammetry and spectrofluorometry. The voltammetric behavior of doxorubicin has been investigated at glassy carbon electrode using differential pulse voltammetry. Doxorubicin is reduced, yielding one reduction peak. Both UV-Vis spectrophotometry and differential pulse voltammetry studies confirm the intercalation reaction. The results showed that both doxorubicin and the MB molecule could intercalate into the double helix of the DNA. The apparent binding constant of doxorubicin with DNA has been found to be 3.2 × 10 4 L mol -1 . The fluorescence signal of doxorubicin and methylene blue was quenched with DNA addition. The Stern-Volmer equation was plotted based on quenching fluorescence signal of doxorubicin.Keywords: doxorubicin, DNA, chemotherapy, spectrophotometry, voltammetry, spectrofluorometry
IntroductionStudy of interactions between drugs and DNA is very interesting and significant not only in understanding the mechanism of interaction, but also for the design of new drugs. 1,2 However mechanism of interactions between drug molecules and DNA is still relatively little known. It is necessary to introduce more simple methods for investigating the mechanism of interaction. By understanding the mechanism of interaction, designing of new DNA-targeted drugs and the screening of these in vitro will be possible.A great variety of substances, including several agents of importance in cancer chemotherapy, 3 are known to bind to DNA by intercalation. 4 Attention has been concentrated on the classical intercalating drugs, acridines and ethidium bromide. [4][5][6] Studies on the binding of various dyes, drugs and antibiotics to DNA and chromatin have contributed to the understanding of the structure of these macromolecules, 6-14 and have suggested possible mechanisms of the biological activity of some drugs. 3 Molecular models of the intercalation of some drugs into DNA have been describ...
“…Interaction between DNA and drug molecules is of current general interest and importance, 1,2 especially for the designing of new DNA-targeted drugs and the screening of these in vitro.…”
Com base em nossa investigação, ambos os complexos, morin-Bi(III) e Morin, podem vincularse ao DNA, embora a natureza da ligação seja diferente para cada um deles. Na presença e ausência do DNA, o morin-Bi(III) mostrou características espectrais diferentes, o que está de acordo com as observadas para outros intercaladores. Neste trabalho, a interação do complexo morin-Bi(III) com o DNA de timo de vitela foi investigada com o uso do azul de metileno (MB), como uma sonda de corante espectral e aplicação de espectrofotometria UV-Vis, espectroscopia de fluorescência e voltametria cíclica. , enquanto que o morin liga-se por um modelo de não-intercalação.Based on our investigation, although both morin-Bi(III) complex and morin can bind to DNA, the nature of the binding was found to be different for each of them. In the presence and absence of the DNA, the morin-Bi(III) complex shows different spectral characteristics which agree with those observed for other intercalators. In this work, the interaction of morin-Bi(III) complex with calf thymus DNA was investigated with the use of methylene blue (MB) dye as a spectral probe and application of UV-Vis spectrophotometry, fluorescence spectroscopy and cyclic voltammetry. The 2:1 morin-Bi(III) complex ratio was calculated by UV-Vis spectroscopy (mole ratio method). The fluorescence signal of Bi(III)-morin complex is increased with DNA addition whereas the fluorescence signal of Morin is decreased with DNA addition. The fluorescence signal of the DNA-complex is quenched by addition of MB which confirms the displacement of the complex with MB. Cyclic voltammetry studies confirm the intercalation reaction. The results showed that only morin-Bi(III) complex can intercalate into the double helix of the DNA. The apparent binding constant of morin-Bi(III) complex with DNA is found to be 2.8 × 10 4 L mol -1, while morin binds in a non-intercalation mode.
“…In addition, some chemical properties make these compounds well suited as alternatives to platinum-based antitumor drugs, such as the rate of ligand exchange, the range of accessible oxidation states, and the ability of ruthenium to mimic iron in binding to certain biological molecules. Hence, complexes based on ruthenium have been proposed to have potential antitumor and antimetastatic activities and generally show lower systemic toxicity than platinum compounds [13].…”
Ruthenium complexes have attracted much attention as possible building blocks for new transition-metal-based antitumor agents. The present study examines the mitotoxic and clastogenic effects induced in the root tips of Allium cepa by cis-tetraammine(oxalato)ruthenium(III) dithionate {cis-[Ru(C(2)O(2))(NH(3))(4)](2)(S(2)O(6))} at different exposure durations and concentrations. Correlation tests were performed to determine the effects of the time of exposure and concentration of ruthenium complex on mitotic index (MI) and mitotic aberration index. A comparison of MI results of cis-[Ru(C(2)O(2))(NH(3))(4)](2)(S(2)O(6)) to those of lead nitrate reveals that the ruthenium complex demonstrates an average mitotic inhibition eightfold higher than lead, with the frequency of cellular abnormalities almost fourfold lower and mitotic aberration threefold lower. A. cepa root cells exposed to a range of ruthenium complex concentrations did not display significant clastogenic effects. Cis-tetraammine(oxalato)ruthenium(III) dithionate therefore exhibits a remarkable capacity to inhibit mitosis, perhaps by inhibiting DNA synthesis or blocking the cell cycle in the G2 phase. Further investigation of the mechanisms of action of this ruthenium complex will be important to define its clinical potential and to contribute to a novel and rational approach to developing a new metal-based drug with antitumor properties complementary to those exhibited by the drugs already in clinical use.
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