Abstract
Oxidative stress-induced gene expression in liver of the untreated newbornc14CoS/c14CoSmouse, as compared with that in thecch/cchwild-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 of14CoS/14CoSmice as compared with that inch/chmice: microsomal aldehyde dehydrogenase (Ahd3) and hepatocyte-specific nuclear factor-1α HNF-1α (Hnfl α). In liver plus nine extrahepatic tissues of untreated newborn14CoS/14CoSmutant andch/chwild-type mice, we compared NMO1, UGT1A6, AHD3 and HNF-1α 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 between14CoS/14CoSandch/chmice.
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