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8638433 
Journal Article 
Extrahepatic expression of NAD(P)H:menadione oxidoreductase, UDP glucuronosyltransferase-1A6, microsomal aldehyde dehydrogenase, and hepatic nuclear factor-1 alpha mRNAs in ch/ch and 14CoS/14CoS mice 
Vasiliou, V; Reuter, SF; Nebert, DW 
1997 
Yes 
Biochemical and Biophysical Research Communications
ISSN: 0006-291X
EISSN: 1090-2104 
233 
3 
631-636 
English 
9168903 
WOS:A1997WX53800010 
Oxidative stress-induced gene expression in liver of the untreated newborn c14CoS/c14CoS mouse, as compared with that in the cch/cch wild-type mouse, appears to be caused by homozygous loss of the fumarylacetoacetate hydrolase (Fah) gene on Chr 7 and absence of the FAH enzyme, which leads to increased levels of endogenous reactive oxygenated metabolites (ROMs) formed in the tyrosine degradative pathway. In these mice almost all studies to date have been carried out in liver. We have examined the extrahepatic expression of four genes. Two genes are members of the [Ah] battery and induced by ROM-mediated oxidative stress: NAD(P)H:menadione oxidoreductase (Nmo1) and UDP glucuronosyltransferase-1A6 (Ugt1a6). The other two genes are decreased in the livers of 14CoS/ 14CoS mice as compared with that in ch/ch mice: microsomal aldehyde dehydrogenase (Ahd3) and hepatocyte-specific nuclear factor-1 alpha HNF-1 alpha (Hnf1 alpha). In liver plus nine extrahepatic tissues of untreated newborn 14CoS/14CoS mutant and ch/ch wild-type mice, we compared NMO1, UGT1A6, AHD3 and HNF-1 alpha mRNA levels. Our results show a wide variation in extrahepatic tissue-specific expression of all four transcripts and indicate that numerous differences exist in the extrahepatic expression of these genes between 14CoS/14CoS and ch/ch mice.