ライフサイエンスコーパス: NAPQI

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1 NAPQI strongly impaired the ability of topoisomerase IIa

2 NAPQI was a strong topoisomerase II poison and increased

3 een NAPQI and MIF is covalent and produces a NAPQI-modified MIF species with diminished cell binding

4 le ipso adduct between glutathione (GSH) and NAPQI using a combination of techniques including liquid

5 pha released to the medium, GST release) and NAPQI toxicity in isolated liver mitochondria (succinate

6 olite of APAP, N-acetyl-p-benzoquinoneimine (NAPQI), caused the selective inhibition of mitochondrial

7 ne metabolite, N-acetyl-p-benzoquinoneimine (NAPQI), which covalently binds to proteins and other mac

8 ive metabolite N-acetyl-p-benzoquinoneimine (NAPQI), which may disrupt the repression of Nrf2 through

9 The reaction between NAPQI and MIF is covalent and produces a NAPQI-modified

10 ate "twin" ion peaks of peptides adducted by NAPQI and for shotgun proteomics via tandem mass spectro

11 l, we demonstrate that activation of Nrf2 by NAPQI and a panel of probe molecules [dexamethasone 21-m

12 the cytotoxic/genotoxic events triggered by NAPQI are consistent with the actions of topoisomerase I

13 At low doses, NAPQI is efficiently detoxified, principally by conjugat

14 (<3 microM) readily accepted electrons from NAPQI-altered, succinate-energized complex II and transf

15 Decomposition kinetics of the GSH-NAPQI ipso adduct and product ratios suggested that the

16 ve metabolite N-acetyl-p-benzoquinone-imide (NAPQI) (r= 0.739;P= 0.058).

17 formation of N-acetyl-p-benzoquinone imine (NAPQI) via induction of cytochrome P450 2E1 (CYP2E1).

18 N-acetyl-p-benzoquinone imine (NAPQI), a reactive metabolite of acetaminophen (APAP), c

19 n metabolite, N-acetyl-p-benzoquinone imine (NAPQI), covalently binds to the active site of MIF.

20 cetaminophen, N-acetyl-p-benzoquinone imine (NAPQI), inhibits both the isomerase and the biological a

21 ve metabolite N-acetyl-p-benzoquinone imine (NAPQI).

22 c metabolite, N-acetyl-p-benzoquinone imine (NAPQI).

23 ports that location dependent differences in NAPQI (the reactive metabolite) formation within hepatic

24 etabolite) formation within hepatic lobules (NAPQI zonation) are necessary and sufficient prerequisit

25 n overdose may be mediated by the actions of NAPQI as a topoisomerase II poison.

26 reactions of cysteinyl thiol ipso adducts of NAPQI provides significant new insights into possible re

27 Partial inhibition of NAPQI formation by CYP2E1 inhibitor diethyldithiocarbama

28 addition to its effects in purified systems, NAPQI appeared to increase levels of DNA scission mediat

29 In this study, kinetic data indicate that NAPQI inhibits MIF both covalently and noncovalently.

30 Here, we show that NAPQI can directly activate the Nrf2 pathway in mouse li

31 more, mass spectrometric analysis shows that NAPQI selectively modifies cysteine residues in Keap1, b

32 t APAP-induced liver injury by bypassing the NAPQI-altered mitochondrial complex II, thus alleviating

33 F cocrystallized with NAPQI reveals that the NAPQI has undergone a chemical alteration forming an ace

34 ata are consistent with a model by which the NAPQI reacts with the catalytic Pro-1 of MIF to disrupt

35 e ipso adduct was readily reversible back to NAPQI under neutral and basic conditions.

36 p were approximately 50% more susceptible to NAPQI (25-165 micromol/L) induced SDH inactivation.

37 The structure of MIF cocrystallized with NAPQI reveals that the NAPQI has undergone a chemical al

38 ming of the changes and the correlation with NAPQI production are consistent with mechanisms known to

39 Whereas treatment with NAPQI, the reactive metabolite of acetaminophen, or the

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