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Studies from Montana State University further understanding of enzyme research
December 17th, 2007
2007 DEC 17 -- "Thioredoxin reductases (Txnrd) maintain intracellular redox homeostasis in most organisms. Metazoan Txnrds also participate in signal tramsduction," scientists writing in the journal Free Radical Biology and Medicine report. "Mouse embryos homozygous for a targeted null mutation of the tynrd1 gene, encoding the cytosolic thioredoxin reductase, were viable at embryonic day 8.5 (E8.5) but not at E9.5. Histology revealed that txnrdl(-/-) cells were capable of proliferation and differentiation,- however, inutant embryos were smaller than wild-type littermates and failed to gastrulate. In situ marker gene analyses indicated that primitive streak mesoderm did not form. Microarray analyses on E7.5 txnrd(-/-) and txnrd(+/+) littermates showed similar mRNA levels for peroxiredoxins, glutathione reductases, rnitochondrial Txnrd2, and most markers of cell proliferation. Conversely, mRNAs encoding suffiredoxin, IGF-binding protein 1, carbonyl reductase 3, glutamate cysteine ligase, glutathione S-transferases, and metallothioneins were more abundant in mutants. Many gene expression responses murrored those in thioredoxin reductase 1-null yeast; however, mice exhibited a novel response within the peroxiredoxin catalytic cycle. Thus, whereas yeast induce peroxiredoxin mRNAs in response to thioredoxin reductase disruption, mice induced sulfiredoxin mRNA. In summary, Txnrd1 was required for correct patterning of the early embryo and progression to later development," wrote A.A. Bondareva and colleagues, Montana State University. The researchers concluded: "Conserved responses to Txnrd1 disruption likely allowed proliferation and limited differentiation of the mutant embryo cells." Bondareva and colleagues published their study in Free Radical Biology and Medicine (Effects of thioredoxin reductase-1 deletion on embryogenesis and transcriptome. Free Radical Biology and Medicine, 2007;43(6):911-923). Additional information can be obtained by contacting E.E. Schmidt, Montana State University, VMB, 960 Technology Blvd., Bozeman, MT 59718, USA. The publisher of the journal Free Radical Biology and Medicine can be contacted at: Elsevier Science Inc., 360 Park Avenue South, New York, NY 10010-1710, USA. Keywords: United States, Bozeman, Dietary Supplement, Enzyme Research, Glutathione, Histology, Micronutrient, RNA Research, Reductase, Therapy, Thioredoxin, Treatment, Montana State University. This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2007, Biotech Business Week via NewsRx.com.
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