کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1270843 | 1496913 | 2014 | 6 صفحه PDF | دانلود رایگان |
• Gemcitabine has no redox activity.
• Gemcitabine-DNA interaction evaluated with a DNA-electrochemical biosensor.
• Variation and occurrence of new DNA oxidation peaks.
• Gemcitabine caused condensation of dsDNA.
• Gemcitabine caused release of guanine residues and formation of abasic sites.
The electrochemical behaviour of the cytosine nucleoside analogue and anti-cancer drug gemcitabine (GEM) was investigated at glassy carbon electrode, using cyclic, differential pulse and square wave voltammetry, in different pH supporting electrolytes, and no electrochemical redox process was observed. The evaluation of the interaction between GEM and DNA in incubated solutions and using the DNA-electrochemical biosensor was studied. The DNA structural modifications and damage were electrochemically detected following the changes in the oxidation peaks of guanosine and adenosine residues and the occurrence of the free guanine residues electrochemical signal. The DNA–GEM interaction mechanism occurred in two sequential steps. The initial process was independent of the DNA sequence and led to the condensation/aggregation of the DNA strands, producing rigid structures, which favoured a second step, in which the guanine hydrogen atoms, participating in the C–G base pair, interacted with the GEM ribose moiety fluorine atoms.
Journal: Bioelectrochemistry - Volume 99, October 2014, Pages 40–45