title: Effects of dietary selenium on post-ischemic expression of antioxidant mRNA.
abstract: Cardiac ischemia reperfusion leads to oxidative stress and poor physiological recovery. Selenium deficiency down-regulates thioredoxin reductase (Txnrd) and glutathione peroxidase (Gpx) activity, impairing recovery from ischemia-reperfusion. Furthermore, selenium supplementation has been shown to be cardioprotective and lessens oxidative stress in reperfused rat hearts. In this study we have investigated the role of selenium in the mRNA expression of these, and related antioxidant proteins, post ischemia-reperfusion. Male rats were fed varying doses of selenium for five weeks. Hearts were isolated and perfused using the Langendorff method with 22.5 min of global ischemia and 45 min reperfusion. RNA was extracted for quantitative real-time PCR analysis of glutathione peroxidase (Gpx)-1 and 4, glutathione reductase (Gsr), thioredoxin peroxidase-2 (Prdx2), thioredoxin (Txn) and thioredoxin reductase (Txnrd)-1 and 2 gene expression. Selenium deficiency produced significant reductions in Gpx-1, Gpx-4, Prdx2, Txnrd-1 and Txnrd-2 expression. Conversely, selenium supplementation of 1000 microg/kg significantly up-regulated Gpx-1, Gpx-4, Txn, Txnrd-1 and Txnrd-2 transcription. Our results show selenium modulates the cardiac mRNA expression of thioredoxin and glutathione related enzymes post ischemia-reperfusion, and impacts on tolerance to ischemia-reperfusion.
authors.affiliation: Heart Foundation Research Centre, School of Health Science, Griffith University Gold Coast Campus, Southport, Australia.
authors.forename: Kylie
authors.initials: K
authors.lastname: Venardos
authors.forename: Kevin
authors.initials: K
authors.lastname: Ashton
authors.forename: John
authors.initials: J
authors.lastname: Headrick
authors.forename: Anthony
authors.initials: A
authors.lastname: Perkins
mesh_terms: D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D001835:Body Weight; D018076:DNA, Complementary / Q000378:metabolism; D004032:Diet; D015536:Down-Regulation; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000096:biosynthesis / Q000378:metabolism; D005980:Glutathione Reductase / Q000096:biosynthesis; D007511:Ischemia / Q000473:pathology*; D008297:Male; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress; D010477:Perfusion; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D012313:RNA / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012643:Selenium / Q000378:metabolism / Q000494:pharmacology*; D013696:Temperature; D013880:Thioredoxin-Disulfide Reductase / Q000096:biosynthesis; D014158:Transcription, Genetic; D000094765:Glutathione Peroxidase GPX1
chemical_list: D000975:Antioxidants; D018076:DNA, Complementary; D012333:RNA, Messenger; D012313:RNA; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D013880:Thioredoxin-Disulfide Reductase; D005978:Glutathione; D012643:Selenium; D000094765:Glutathione Peroxidase GPX1; C000722069:Gpx1 protein, rat