RESUMO
Pulmonary rehabilitation (PR) improves physical capacity and health quality in patients with chronic obstructive pulmonary disease (COPD). However, the effect of exercise on oxidative stress markers in COPD patients is only partially known. This study was designed to evaluate the oxidative stress response to long-term exercise in patients with COPD enrolled in a PR program. Fifteen COPD patients (FEV1 < 60%), age between 50 and 60 years, ex-smokers, were separated in two groups: exercise-trained (n=8) and sedentary group (n=7). Exercise consisted of an 8-week conditioning program using a cycle ergometer (three times a week, 1h session). An endurance test (60% of maximal load in an incremental cycle test) was performed before and after PR. Blood samples were obtained at baseline and immediately after each endurance test. We measured the index of lipid peroxidation, thiobarbituric acid reactive species (TBARS), total radical-trapping antioxidant parameter (TRAP) and xanthine oxidase (XO) activity. TRAP was significantly different between the exercise-trained group and sedentary group of COPD patients. Baseline TBARS values were increased after the exercise training program but decreased after the endurance test. XO decrease after effort in the trained and untrained groups. The results suggest that patients with COPD are characterized by increased systemic and pulmonary oxidative stress markers both at rest as well as induced by cardiopulmonary exercise test and that PR program was associated with decreased systemic exercise-induced oxidative damage.
Assuntos
Terapia por Exercício , Estresse Oxidativo , Doença Pulmonar Obstrutiva Crônica/reabilitação , Testes Respiratórios , Humanos , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/metabolismo , Testes de Função RespiratóriaRESUMO
In this study we compared the antioxidant properties of five different extracts of different composition obtained from Achyrocline satureioides' inflorescences (Compositae), a widely used Brazilian folk medicinal herb. All of the extracts presented significant antioxidant potential identified by TRAP assay, which increased in the presence of human plasma. Characterization of the content of flavonoids in each extract showed that the FDP80 (ethanol 80%) and FFr (enriched flavonoid fraction) extracts contained a higher content of flavonoids. Cytotoxicity of the extracts as determined in Sertoli cell culture showed that FDP80 and FFr were highly toxic at most concentrations tested. The extracts induced a significant increase in lipid peroxidation levels in Sertoli cells. These results suggest that medicinal herb extracts that contain higher flavonoid concentrations and shows higher antioxidant protection in vitro might not always produce the greatest benefit.
Assuntos
Achyrocline/química , Antioxidantes/farmacologia , Extratos Vegetais/farmacologia , Células de Sertoli/efeitos dos fármacos , Animais , Brasil , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Cromatografia Líquida de Alta Pressão , Relação Dose-Resposta a Droga , Flavonoides/análise , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Extratos Vegetais/química , Plantas Medicinais/química , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio/farmacologia , Células de Sertoli/patologia , Substâncias Reativas com Ácido TiobarbitúricoRESUMO
Oxidative stress and excess of iron in the brain has been implicated in a variety of acute and chronic neurological conditions. The neonatal period is critical for the establishment of normal iron content in the adult brain. In the present study, the long-term oxidative effects of iron exposure during this period were assessed by treating Wistar rats orally with 0, 7.5 or 15 mg Fe(+2)/kg of body weight on postnatal days 10-12. Thiobarbituric acid reactive species, protein carbonyl, superoxide dismutase activity were measured at the age of 3 months. It was found that there was an increase in thiobarbituric acid reactive species and protein carbonyl in the substantia nigra of iron treated rats. In contrast, oxidative stress in the striatum was decreased. Superoxide dismutase activity was decreased in the substantia nigra iron treated rats. There were no differences in cerebellum measures among the groups. Our results demonstrated that iron supplementation in a critical neonatal period induced oxidative stress and modulated SOD activity in the adult life in selective brain regions.
Assuntos
Ferro/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Substância Negra/efeitos dos fármacos , Substância Negra/metabolismo , Fatores Etários , Animais , Animais Recém-Nascidos , Cerebelo/efeitos dos fármacos , Cerebelo/metabolismo , Corpo Estriado/efeitos dos fármacos , Corpo Estriado/metabolismo , Feminino , Masculino , Doença de Parkinson/metabolismo , Gravidez , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismoRESUMO
Prion diseases are fatal neurodegenerative disorders resulting from conformational changes in the prion protein from its normal cellular isoform, PrPC, to the infectious scrapie isoform, PrP(Sc). In spite of many studies, the physiological function of PrPC remains unknown. Recent work shows that PrPC binds Cu2+, internalizing it into the cytoplasm. Since many antioxidant enzymes depend on Cu2+ (e.g., Cu/ZnSOD), their function could be affected in prion diseases. Here we investigate a possible relationship between PrP(C) and the cellular antioxidant systems in different structures isolated from PrPC knockout and wild-type mice by determining oxidative damage in protein and lipids and activity of antioxidant enzymes (CAT, SOD) and stress-adaptive enzymes (ODC). Our results show that, in the absence of PrPC, there is an increased oxidation of lipid and protein in all structures investigated. Decreased SOD activity and changes in CAT/ODC activities were also observed. Taking into account these results, we suggest that the physiological function of PrP(C) is related to cellular antioxidant defenses. Therefore, during development of prion diseases, the whole organism becomes more sensitive to ROS injury, leading to a progressive oxidative disruption of tissues and vital organs, especially the central nervous system.