Camiletti Moirón, DanielAparicio, VictoriaNebot Valenzuela, ElenaMedina, GerardoMartínez, RosarioKapravelou, GaryfalliaAndrade, AnaPorres, JesúsLópez Jurado, MaríaAranda, Pilar2024-01-302024-01-302015Daniel Camiletti-Moirón, Virginia Aparicio, Elena Nebot, Gerardo Medina, Rosario Martínez, Garyfallia Kapravelou, Ana Andrade, Jesús Porres, Maria Lopez-Jurado, and Pilar Aranda Ramírez. High-intensity exercise modifies the effects of Stanozolol on brain oxidative stress in rats. International Journal of Sports Medicine. 2015 Mar 14; 36(10):1-8.0172-462210.1055/s-0035-1548941https://hdl.handle.net/20.500.14352/96367We analyzed the effects of high-intensity exercise (HIE) and anabolic androgenic steroids (AAS) on brain redox status. 40 male Wistar rats were randomly distributed in 4 experimental groups (n=10) with or without HIE and with or without weekly Stanozolol administration. Thiobarbituric acid-reactive substances (TBARs) and protein carbonyl content (PCC) were assessed. Total superoxide dismutase (tSOD), manganese superoxide dismutase (Mn-SOD), copper/zinc superoxide dismutase (CuZn-SOD) and catalase (CAT) activities were measured. Finally, protein expression levels of glutathione peroxidase (GPx), NAD(P)H dehydrogenase, Quinone 1 (NQO1), NF-E2-Related Factor 2 (Nrf2), glial fibrillary acidic protein (GFAP), nuclear factor kappa β p65 (NF-κβ) and signal transducer and activator of transcription 3 were determined. Brain PCC concentrations were lower in the HIE groups compared to the untrained controls, whereas CAT activity was higher (both, p<0.01). Both HIE and AAS groups exhibited higher expression levels of GFAP and GPx, but lower NQO1 levels (all, p<0.05). There were increased expression levels of NF-κβ in the AAS groups (p<0.01). In addition, there was increased expression of Nrf2 in the HIE groups (p<0.001). HIE*AAS interactions were found on TBARs content and GFAP expression, with HIE downregulating and upregulating AAS-mediated increases in TBARs and GFAP, respectively (p<0.05). Overall, HIE appeared to reduce the AAS-mediated negative effect on brain redox status.engjournal article1439-3964https://doi.org/10.1055/s-0035-1548941https://pubmed.ncbi.nlm.nih.gov/26252547/restricted access612Anabolic agentsSuperoxide dismutaseCatalaseGlial fibrillary acidic proteinNuclear factor kappa βResistance trainingFisiología2411 Fisiología Humana