title: Oxidative stress in leukocytes from young prematurely aging mice is reversed by supplementation with biscuits rich in antioxidants.
abstract: Aging is associated with a progressive dysregulation of immune responses as a result of increased oxidative stress. Therefore, we have assessed the oxidative stress status of peritoneal leukocytes from young prematurely aging mice (PAM) as compared with non-prematurely aging mice (NPAM), as well as the effects on this oxidative stress of a dietary supplementation with biscuits rich in antioxidants (vitamin C, vitamin E, beta-carotenes, zinc and selenium). We found that, in the peritoneal leukocytes, the levels of several parameters of oxidation such as extracellular superoxide anion (O(2)(-)), Prostaglandin E(2) (PGE(2)), nitric oxide, oxidized glutathione (GSSG) and lipid peroxidation (malondialdehyde, MDA) were higher in PAM as compared with NPAM, whereas the antioxidant defences such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) activities, as well as reduced glutathione (GSH) levels, were decreased. Consequently, young PAM showed an oxidative stress in their leukocytes, which is characteristic of mice of an older chronological age. Antioxidant diet supplementation was able to restore redox homeostasis, increasing the antioxidant and decreasing the oxidant levels. Accordingly, supplementation with adequate levels of antioxidants, from an early age, could be useful to preserve health, especially in prematurely aging populations.
authors.affiliation: Department of Physiology, Animal Physiology II, Faculty of Biological Sciences, Complutense University, 28040 Madrid, Spain.
authors.forename: Carmen
authors.initials: C
authors.lastname: Alvarado
authors.forename: Pedro
authors.initials: P
authors.lastname: Alvarez
authors.forename: Liliana
authors.initials: L
authors.lastname: Jiménez
authors.forename: Mónica
authors.initials: M
authors.lastname: De la Fuente
mesh_terms: D000375:Aging / Q000097:blood* / Q000276:immunology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002374:Catalase / Q000097:blood; D015232:Dinoprostone / Q000097:blood; D005260:Female; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D005980:Glutathione Reductase / Q000097:blood; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000276:immunology*; D008315:Malondialdehyde / Q000097:blood; D051379:Mice; D008813:Mice, Inbred ICR; D009569:Nitric Oxide / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects; D011897:Random Allocation; D013047:Specific Pathogen-Free Organisms; D013482:Superoxide Dismutase / Q000097:blood; D013481:Superoxides / Q000097:blood
chemical_list: D000975:Antioxidants; D013481:Superoxides; D009569:Nitric Oxide; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione; D015232:Dinoprostone