Literature DB >> 2379326

Temporal expression of genes encoding free radical-metabolizing enzymes is associated with higher mRNA levels during in utero development in mice.

S el-Hage1, S M Singh.   

Abstract

The interaction of reactive oxygen metabolites with DNA is well characterized and may result in mutagenesis, chromosome aberrations, and modulation of gene expression. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) catalyze enzymatic reactions to remove oxidant stresses, particularly O2- and H2O2. The role of these enzymes during in utero development of the embryo and the developmental pattern of expression of the embryonic genes encoding them is not known. We examined the in utero developmental expression and activity of the three free-radical-metabolizing enzymes in mice. We collected mouse fetuses at different stages of development and examined total RNA populations by Northern and slot blots using gene-specific cDNA probes. In addition to quantifying the probe-specific RNAs, activities of the three enzymes were also evaluated on the same tissue samples. The gene-specific RNAs and the associated enzyme activities are detectable with somite formation (day 8 postcoitus [p.c.]) in mice. The relative RNA values for each of the genes studied are higher in in utero stages as compared with the adult. The specific activities of these enzymes, on the other hand, follow a characteristic increase with development and growth. The relative RNA levels for each of the genes studied are higher during in utero growth and development than the relative enzyme activity values (between day 8 and day 18, third trimester) in the liver and carcass. This may suggest that the mRNA specific to these genes may accumulate in utero and are not translated immediately. Such accumulating transcripts are translated efficiently after birth, when these enzymes are particularly needed with the advent of aerobic respiration.

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Year:  1990        PMID: 2379326     DOI: 10.1002/dvg.1020110205

Source DB:  PubMed          Journal:  Dev Genet        ISSN: 0192-253X


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