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1 reated with a selective inhibitor of NQO(1), dicumarol.
2 enten kinetics and was markedly inhibited by dicumarol, a competitive inhibitor of naphthoquinone oxi
9 vity is insensitive to rotenone, flavone, or dicumarol; however, it was inhibited by diphenyl iodoniu
11 atalase with adenoviral vectors reversed the dicumarol-induced cytotoxicity and reversed fluorescence
14 ibitable NAD(P)H:menadione oxidoreductase or dicumarol-inhibitable NAD(P)H:dichlorophenolindophenol r
15 ified DT-diaphorase can be assayed as either dicumarol-inhibitable NAD(P)H:menadione oxidoreductase o
16 When DT-diaphorase activity was measured as dicumarol-inhibitable NADPH:dichlorophenolindophenol red
19 ctase NAD(P)H:quinone oxidoreductase (NQO1), dicumarol is also thought to affect quinone-mediated ele
20 H, or NMNH; (ii) is very weakly inhibited by dicumarol or Cibacron blue; (iii) is very potently inhib
22 inone oxidoreductase enzymatic activity with dicumarol prior to quinone treatment resulted in increas
23 using mitomycin (trial 1) and mitomycin with dicumarol (trial 2) as an adjunct to radiation therapy i
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