Document Detail


Redox cycling of 9,10-phenanthraquinone to cause oxidative stress is terminated through its monoglucuronide conjugation in human pulmonary epithelial A549 cells.
MedLine Citation:
PMID:  18294972     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
9,10-Phenanthraquinone (PQ), a component of airborne particulate matter, causes marked cellular protein oxidation and cytotoxicity through a two-electron reduction to 9,10-dihydroxyphenanthrene (PQH2), which is associated with the propagation of reactive oxygen species (K. Taguchi et al., Free Radic. Biol. Med. 43:789-799, 2007). In the present study, we explored a biotransformation pathway for the detoxification of PQ. Exposure of human pulmonary epithelial A549 cells to PQ resulted in a time-dependent appearance of an unknown metabolite in the medium that was identified as the monoglucuronide of PQH2 (PQHG). Whereas a variety of isozymes of uridine 5'-diphosphate glucuronosyltransferase (UGTs) are responsible for PQHG formation, UGT1A10 and UGT1A6 were particularly effective catalysts for glucuronide conjugation. In cell-free systems, PQ exhibited a rapid thiol oxidation and subsequent oxygen consumption in the presence of dithiothreitol, whereas PQHG did not. Unlike the parent compound, PQHG completely lost the ability to oxidize cellular proteins and cause cell death in A549 cells. In addition, deletion of the transcription factor Nrf2 decreased PQHG formation and increased PQ-mediated toxicity of mouse primary hepatocytes. Thus, we conclude that PQHG is a metabolite of PQ, generated through PQH2, that terminates its redox cycling and transports it to extracellular space.
Authors:
Keiko Taguchi; Megumi Shimada; Sayako Fujii; Daigo Sumi; Xiaoqing Pan; Shigeru Yamano; Takahito Nishiyama; Akira Hiratsuka; Masayuki Yamamoto; Arthur K Cho; John R Froines; Yoshito Kumagai
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2008-02-09
Journal Detail:
Title:  Free radical biology & medicine     Volume:  44     ISSN:  0891-5849     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-04-04     Completed Date:  2008-06-19     Revised Date:  2011-05-19    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1645-55     Citation Subset:  IM    
Affiliation:
Doctoral Programs in Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Epithelial Cells / drug effects,  metabolism*
Glucuronosyltransferase / genetics,  metabolism
Hepatocytes / drug effects,  metabolism
Humans
Intracellular Signaling Peptides and Proteins / genetics,  metabolism
Lung / drug effects,  metabolism
Male
Metabolic Detoxication, Drug
Mice
Mice, Inbred C57BL
Mice, Inbred ICR
NF-E2-Related Factor 2 / genetics,  metabolism
Oxidation-Reduction
Oxidative Stress / drug effects*
Oxygen Consumption / drug effects
Particulate Matter / pharmacokinetics*,  toxicity
Phenanthrenes / pharmacokinetics*,  toxicity
Substrate Specificity
Chemical
Reg. No./Substance:
0/Intracellular Signaling Peptides and Proteins; 0/KEAP1 protein, human; 0/NF-E2-Related Factor 2; 0/Nfe2l2 protein, mouse; 0/Particulate Matter; 0/Phenanthrenes; 84-11-7/9,10-phenanthrenequinone; EC 2.4.1.-/UDP-glucuronosyltransferase, UGT1A6; EC 2.4.1.-/bilirubin uridine-diphosphoglucuronosyl transferase 1A10; EC 2.4.1.17/Glucuronosyltransferase

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