RESUMEN
Jabuticaba has a high concentration of phenolic compounds, which have a significant antioxidant capacity. Methodologies have been developed to evaluate the ability of plant extracts to fight free radicals such as H2O2, O2â¢-, HOCl, ONOO- and ROOâ¢. Thus, the capacity of deactivation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in peel and seed extracts of five varieties of jabuticaba was evaluated. Sabará peel (SFP) deactivated HOCl with IC50 9.24 µg. mL-1; Paulista seed (PF) deactivated O2â¢- with IC50 16.15 µg. mL-1; Coroada seed (CFP) deactivated ONOO- with IC50 3.84 µg. mL-1; the peel of CFP deactivated ONOO- with IC50 5.88 µg. mL-1; the peel of SFP deactivated the ROO⢠at 918.16 µmol TE. g-1; and Sabará seed deactivated H2O2 with 49.11% inhibition at a concentration of 125 µg. mL-1 of extract. These results demonstrate the high antioxidant potential of this fruit, indicating that it could be extremely beneficial to human health.
Asunto(s)
Antioxidantes/farmacología , Myrtaceae/química , Extractos Vegetales/farmacología , Especies de Nitrógeno Reactivo/antagonistas & inhibidores , Especies Reactivas de Oxígeno/antagonistas & inhibidores , Frutas/química , Humanos , Extractos Vegetales/química , Semillas/químicaRESUMEN
Mitochondrial dysfunction characterized by impaired bioenergetics, oxidative stress and aldehydic load is a hallmark of heart failure. Recently, different research groups have provided evidence that selective activation of mitochondrial detoxifying systems that counteract excessive accumulation of ROS, RNS and reactive aldehydes is sufficient to stop cardiac degeneration upon chronic stress, such as heart failure. Therefore, pharmacological and non-pharmacological approaches targeting mitochondria detoxification may play a critical role in the prevention or treatment of heart failure. In this review we discuss the most recent findings on the central role of mitochondrial dysfunction, oxidative stress and aldehydic load in heart failure, highlighting the most recent preclinical and clinical studies using mitochondria-targeted molecules and exercise training as effective tools against heart failure.
Asunto(s)
Antioxidantes/uso terapéutico , Materiales Biomiméticos/uso terapéutico , Cardiotónicos/uso terapéutico , Insuficiencia Cardíaca/terapia , Mitocondrias Cardíacas/efectos de los fármacos , Ubiquinona/análogos & derivados , Aldehídos/antagonistas & inhibidores , Aldehídos/metabolismo , Animales , Ensayos Clínicos como Asunto , Modelos Animales de Enfermedad , Evaluación Preclínica de Medicamentos , Metabolismo Energético/efectos de los fármacos , Ejercicio Físico , Insuficiencia Cardíaca/metabolismo , Insuficiencia Cardíaca/patología , Humanos , Malondialdehído/antagonistas & inhibidores , Malondialdehído/metabolismo , Mitocondrias Cardíacas/metabolismo , Mitocondrias Cardíacas/patología , Estrés Oxidativo/efectos de los fármacos , Especies de Nitrógeno Reactivo/antagonistas & inhibidores , Especies de Nitrógeno Reactivo/metabolismo , Especies Reactivas de Oxígeno/antagonistas & inhibidores , Especies Reactivas de Oxígeno/metabolismo , Superóxido Dismutasa/química , Ubiquinona/uso terapéuticoRESUMEN
A large number of researches have led to a substantial growth of knowledge about exercise and oxidative stress. Initial investigations reported that physical exercise generates free radical-mediated damages to cells; however, in recent years, studies have shown that regular exercise can upregulate endogenous antioxidants and reduce oxidative damage. Yet, strenuous exercise perturbs the antioxidant system by increasing the reactive oxygen species (ROS) content. These alterations in the cellular environment seem to occur in an exercise type-dependent manner. The source of ROS generation during exercise is debatable, but now it is well established that both contracting and relaxing skeletal muscles generate reactive oxygen species and reactive nitrogen species. In particular, exercises of higher intensity and longer duration can cause oxidative damage to lipids, proteins, and nucleotides in myocytes. In this review, we summarize the ROS effects and interplay of antioxidants in skeletal muscle during physical exercise. Additionally, we discuss how ROS-mediated signaling influences physical exercise in antioxidant system.
Asunto(s)
Antioxidantes/uso terapéutico , Ejercicio Físico , Estilo de Vida Saludable , Músculo Esquelético/metabolismo , Estrés Oxidativo , Especies Reactivas de Oxígeno/antagonistas & inhibidores , Daño por Reperfusión/prevención & control , Animales , Antiinflamatorios no Esteroideos/metabolismo , Antiinflamatorios no Esteroideos/uso terapéutico , Antioxidantes/metabolismo , Supervivencia Celular , Dieta Saludable , Suplementos Dietéticos , Humanos , Mitocondrias Musculares/enzimología , Mitocondrias Musculares/inmunología , Mitocondrias Musculares/metabolismo , Fatiga Muscular , Músculo Esquelético/irrigación sanguínea , Músculo Esquelético/inmunología , Músculo Esquelético/fisiopatología , Mialgia/etiología , Mialgia/prevención & control , Miositis/inmunología , Miositis/prevención & control , Consumo de Oxígeno , Esfuerzo Físico , Especies de Nitrógeno Reactivo/antagonistas & inhibidores , Especies de Nitrógeno Reactivo/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Daño por Reperfusión/inmunología , Daño por Reperfusión/metabolismo , Daño por Reperfusión/fisiopatologíaRESUMEN
1. The contribution of nitric oxide (NO) and peroxynitrite (PN) to inflammation in a zymosan-induced (1 mg, intra-articular, i.art.) rat model of arthritis was assessed by histopathology and by measuring the glycosaminoglycan (GAG) content of the articular cartilage. 2. Progression of the chronic synovitis in zymosan-induced arthritis (ZYA) was associated with increased nitrite and nitrotyrosine (3-NT) levels in the joint exudates that paralleled a progressive loss of the GAG content. An increase in 3-NT was also observed after i.art. PN. 3. The nonselective nitric oxide synthase (NOS) inhibitor l-N(G)-nitroarginine methyl ester (25-75 mg x kg(-1)day(-1)) or the selective inducible NOS inhibitor aminoguanidine (50-100 mg x kg(-1)day(-1)) given 1 h before (prophylactic) or 3 days after (therapeutic) injection of the zymosan ameliorated the synovitis, but worsened the GAG loss, as measured at the end of the experiment (day 7). 4. The PN scavenger uric acid (100-250 mg x kg(-1) i.p. four times daily) given prophylactically until the end of the experiment (day 14), in a dose compatible with its PN scavenging activity, significantly decreased both the synovitis and the GAG loss. 5. In conclusion, PN formation is associated with cartilage damage in addition to proinflammatory activity in ZYA. NOS inhibitors and a PN scavenger were able to reduce the cellular infiltration, while displaying opposite effects on cartilage homeostasis either by enhancing or ameliorating the damage, respectively.