title: Oxidative stress in the kidney of reproductive male rats during aging.
abstract: Reproduction alters the male physiology. We performed a comprehensive examination of oxidative stress in the kidneys of male rats with (experienced) or without (naïve) reproductive activity during aging. Oxidative stress was assessed by measuring the activity of catalase, glutathione peroxidase, glutathione S-transferase, and superoxide dismutase, and by measuring protein carbonylation, lipid peroxidation, nitrite and nitrate levels, vitamin C levels, and glutathione (total, reduced, and oxidized forms) levels, and metabolism was accessed by aconitase activity in kidney tissue, as well as testosterone and estradiol levels in serum. Reproductively active animals exhibited increased testosterone levels and altered metabolism. Aging affects tissues and organs and contributes to their functional decline. Elderly naïve rats showed high nitrite and nitrate levels. The experienced rats had less damage in elderly ages, probably because they had higher antioxidant amount and antioxidant enzyme activities at earlier ages, which would have avoided oxidative damage seen in naïve group, and because of the metabolism decline. Glutathione increase in naïve elder rats probably was induced for direct protection against oxidative damage and indirect protection by higher glutathione peroxidase and glutathione S-transferase activities. Linear regression shows that lipid peroxidation levels explained vitamin C levels (B standardized value of 0.42), indicating that vitamin C was properly produced or recruited into kidneys to combat lipid peroxidation. Catalase activity reflected the protein carbonylation and lipid peroxidation levels (B standardized values of 0.28 and 0.48). These results add comprehensive data regarding changes in oxidative stress during aging, and suggest an explanation for the costs of reproduction.
authors.affiliation: Programa de Pós-Graduação em Biologia Celular e Molecular, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
authors.forename: Paulo V G
authors.initials: PV
authors.lastname: Alabarse
authors.forename: Tiago B
authors.initials: TB
authors.lastname: Salomon
authors.forename: Tássia M
authors.initials: TM
authors.lastname: Medeiros
authors.forename: Fernanda S
authors.initials: FS
authors.lastname: Hackenhaar
authors.forename: Artur K
authors.initials: AK
authors.lastname: Schüller
authors.forename: Guilherme
authors.initials: G
authors.lastname: Ehrenbrink
authors.forename: Mara S
authors.initials: MS
authors.lastname: Benfato
mesh_terms: D000375:Aging / Q000378:metabolism*; D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004958:Estradiol / Q000097:blood; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D007668:Kidney / Q000201:enzymology / Q000378:metabolism*; D016014:Linear Models; D015227:Lipid Peroxidation; D008297:Male; D009566:Nitrates / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D018384:Oxidative Stress; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D013739:Testosterone / Q000097:blood
chemical_list: D009566:Nitrates; D009573:Nitrites; D013739:Testosterone; D004958:Estradiol; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D005978:Glutathione; D001205:Ascorbic Acid