title: Optimization of selenium status by a single intraperitoneal injection of Se in Se-deficient rat: possible application to burned patient treatment.
abstract: In order to investigate the efficiency of a single selenium (Se) administration in restoring selenium status, Se and antioxidant enzymes were studied in an animal model of Se depletion. In Se-depleted animals receiving or not a single parenteral administration of Se, plasma, red blood cell (RBC), and tissue Se levels were measured concurrently with glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities. The oxidative stress was assessed by thiobarbituric acid-reactive species (TBARs), total thiol groups, glutathione, and tocopherol measurements. Our study showed that Se depletion with alterations in the antioxidant defense system (Se and GPx activity decreases) led to an increase of lipid peroxidation, a decrease of the plasma vitamin E level, and SOD activation. Sodium selenite injection resulted after 24 h in an optimal plasma Se level and a reactivation of GPx activity. In liver, brain, and kidney, Se levels in injected animals were higher than those in reference animals. However, this single administration of Se failed to decrease free radical damage induced by Se depletion. Therefore, in burned patients who exhibit an altered Se status despite a daily usually restricted Se supplementation, the early administration of a consistent Se amount to improve the GPx activity should be of great interest in preventing the impairment of the antioxidant status.
authors.affiliation: Centre de Recherches du Service de Santé des Armées, 24 Av. du Maquis du Grésivaudan, BP87, 38702 La Tronche cedex, France. diane.agay@crssa.net
authors.forename: Diane
authors.initials: D
authors.lastname: Agay
authors.forename: Caroline
authors.initials: C
authors.lastname: Sandre
authors.forename: Véronique
authors.initials: V
authors.lastname: Ducros
authors.forename: Henri
authors.initials: H
authors.lastname: Faure
authors.forename: Catherine
authors.initials: C
authors.lastname: Cruz
authors.forename: Antonia
authors.initials: A
authors.lastname: Alonso
authors.forename: Anne-Marie
authors.initials: AM
authors.lastname: Roussel
authors.forename: Yves
authors.initials: Y
authors.lastname: Chancerelle
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D002056:Burns / Q000628:therapy*; D004195:Disease Models, Animal; D004912:Erythrocytes / Q000378:metabolism; D005609:Free Radicals; D005979:Glutathione Peroxidase / Q000737:chemistry / Q000378:metabolism; D007274:Injections, Intraperitoneal; D007668:Kidney / Q000378:metabolism; D015227:Lipid Peroxidation; D008099:Liver / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D012643:Selenium / Q000737:chemistry / Q000172:deficiency* / Q000494:pharmacology*; D013438:Sulfhydryl Compounds; D013482:Superoxide Dismutase / Q000737:chemistry / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances; D013997:Time Factors; D014018:Tissue Distribution; D024505:Tocopherols / Q000737:chemistry; D014810:Vitamin E / Q000378:metabolism
chemical_list: D000975:Antioxidants; D005609:Free Radicals; D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D012643:Selenium; D024505:Tocopherols