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2016 ; 80
(ä): 647-653
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Using DNA devices to track anticancer drug activity
#MMPMID26901461
Kahanda D
; Chakrabarti G
; Mcwilliams MA
; Boothman DA
; Slinker JD
Biosens Bioelectron
2016[Jun]; 80
(ä): 647-653
PMID26901461
show ga
It is beneficial to develop systems that reproduce complex reactions of
biological systems while maintaining control over specific factors involved in
such processes. We demonstrated a DNA device for following the repair of DNA
damage produced by a redox-cycling anticancer drug, beta-lapachone (?-lap). These
chips supported ß-lap-induced biological redox cycle and tracked subsequent DNA
damage repair activity with redox-modified DNA monolayers on gold. We observed
drug-specific changes in square wave voltammetry from these chips at therapeutic
ß-lap concentrations of high statistical significance over drug-free control. We
also demonstrated a high correlation of this change with the specific
ß-lap-induced redox cycle using rational controls. The concentration dependence
of ß-lap revealed significant signal changes at levels of high clinical
significance as well as sensitivity to sub-lethal levels of ß-lap. Catalase, an
enzyme decomposing peroxide, was found to suppress DNA damage at a NQO1/catalase
ratio found in healthy cells, but was clearly overcome at a higher NQO1/catalase
ratio consistent with cancer cells. We found that it was necessary to reproduce
key features of the cellular environment to observe this activity. Thus, this
chip-based platform enabled tracking of ß-lap-induced DNA damage repair when
biological criteria were met, providing a unique synthetic platform for
uncovering activity normally confined to inside cells.
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