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1.
Rev. bras. med. esporte ; 25(5): 404-408, Sept.-Oct. 2019. graf
Article in English | LILACS | ID: biblio-1042354

ABSTRACT

ABSTRACT Introduction Obesity is a complex and multifactorial metabolic disorder characterized by the accumulation of body fat; physical exercise increases energy expenditure and promotes a reparative effect through modulation of endogenous antioxidant defenses. Objective To evaluate the effects of the high-fat diet (HFD) on oxidative stress parameters in skeletal muscles of rats using aerobic exercise training protocols (AETP), moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT). Methods The study was quantitative and experimental. Animals received 8 weeks of HFD or normal diet (ND), followed by 9 weeks of HFD or ND and the two AETPs. Results HFD did not alter the formation of thiobarbituric acid reactive substances (TBA-RS), total sulfhydryl and protein carbonyl content in the soleus and plantaris muscles; in contrast, the protocols caused a decrease in TBA-RS levels in the plantaris muscle and increased the sulfhydryl content in the soleus muscle, while MICT increased the sulfhydryl content in the plantaris muscle and reduced protein carbonyl content in both muscles. HFD reduced SOD activity in the plantaris muscle while the MICT protocol enhanced SOD in the soleus muscle and both protocols reversed the decrease in SOD in the plantaris muscle. HFD increased CAT activity in the soleus muscle, the HIIT protocol prevented this alteration and both protocols increased CAT in the plantaris muscle. HFD reduced GSH-Px activity in both muscles, and the MICT protocol prevented this reduction in the soleus muscle, while the HIIT protocol partially prevented this decrease. The MICT protocol did not prevent the reduction of GSH-Px and the HIIT protocol partially prevented this decrease in the plantaris muscle. Conclusions HFD elicited oxidative stress in the skeletal muscle of rats, and both protocols were able to prevent most of the alterations in oxidative stress parameters caused by the HFD. Level of evidence IV; Investigation of treatment outcomes.


RESUMO Introdução Obesidade é uma desordem metabólica complexa e multifatorial, caracterizada pelo acúmulo de gordura corporal. O exercício físico tem a capacidade de aumentar o gasto energético e promover efeito reparador por meio da modulação das defesas antioxidantes endógenas. Objetivo Avaliar os efeitos da dieta hiperlipídica (DHL) sobre parâmetros de estresse oxidativo em músculos esqueléticos de ratos, por protocolos de treinamento físico aeróbico (TFA), treinamento contínuo de intensidade moderada (TCIM) e treinamento intervalo de alta intensidade (HIIT). Métodos O estudo foi quantitativo e experimental. Animais receberam 8 semanas de DHL ou dieta normal (DN), seguidas por 9 semanas de DHL ou DN e os dois TFA. Resultados A DHL não alterou a formação de substâncias reativas ao ácido tiobarbitúrico (TBA-RS), conteúdo total de sulfidrilas e de proteínas carboniladas nos músculos sóleo e plantar. Em contraste, os protocolos diminuíram TBA-RS no músculo plantar e aumentaram o conteúdo de sulfidrilas no músculo sóleo. TCIM aumentou o conteúdo de sulfidrilas no músculo plantar e reduziu o conteúdo de proteínas carboniladas em ambos os músculos. A DHL reduziu a atividade da SOD no músculo plantar; o TCIM aumentou a SOD no músculo sóleo e ambos os protocolos reverteram a diminuição da SOD no músculo plantar. A DHL aumentou a CAT no músculo sóleo, o HIIT preveniu essa alteração e ambos os protocolos aumentaram a CAT no músculo plantar. A DHL diminuiu a atividade da GSH-Px em ambos os músculos, e o TCIM preveniu esta diminuição no músculo sóleo, enquanto que o HIIT preveniu parcialmente esta diminuição. O TCIM não preveniu a redução da GSH-Px, e o HIIT preveniu parcialmente esta diminuição no músculo plantar. Conclusão A DHL causou estresse oxidativo nos músculos esqueléticos de ratos, e ambos os protocolos foram capazes de prevenir a maioria das alterações nos parâmetros de estresse oxidativo causadas pela DHL. Nível de evidência IV; Investigação dos resultados do tratamento.


RESUMEN Introducción La obesidad es un desorden metabólico complejo y multifactorial caracterizado por la acumulación de grasa corporal. El ejercicio físico tiene la capacidad de aumentar el gasto energético y promover efecto reparador por medio de la modulación de las defensas antioxidantes endógenas. Objetivos Evaluar los efectos de la dieta hiperlipídica (DHL) sobre parámetros de estrés oxidativo en los músculos esqueléticos de las ratas, por protocolos de entrenamiento físico aeróbico (TFA), entrenamiento continuo de intensidad moderada (TCIM) y entrenamiento de intervalo de alta intensidad (HIIT). Métodos El estudio fue cuantitativo y experimental. Los animales recibieron ocho semanas de DHL o dieta normal (DN), seguidas por nueve semanas de DHL o DN y los dos TFA. Resultados La DHL no alteró la formación de sustancias reactivas al ácido tiobarbitúrico (TBA-RS), contenido total de sulfhidrilos y de proteínas carboniladas en los músculos sóleo y plantar. En contraste, los protocolos disminuyeron TBA-RS en el músculo plantar y aumentaron el contenido de sulfhidrilos en el músculo sóleo. TCIM aumentó el contenido de sulfhidrilos en el músculo plantar y redujo el contenido de proteínas carboniladas en ambos músculos. La DHL redujo la actividad de la SOD en el músculo plantar, el TCIM aumentó la SOD en el músculo sóleo y ambos protocolos revirtieron la disminución de la SOD en el músculo plantar. La DHL aumentó la CAT en el músculo sóleo, el HIIT previno esa alteración y ambos protocolos aumentaron la CAT en el músculo plantar. La DHL disminuyó la actividad de GSH-Px en ambos músculos, y el TCIM previno esta disminución en el músculo sóleo, mientras que el HIIT previno parcialmente esta disminución. El TCIM no previno la reducción de la GSH-Px y el HIIT previno parcialmente esta disminución en el músculo plantar. Conclusión La DHL causó estrés oxidativo en los músculos esqueléticos de ratones y ambos protocolos fueron capaces de prevenir la mayoría de las alteraciones en los parámetros de estrés oxidativo causados por DHL. Nivel de evidencia IV; Investigación de los resultados del tratamiento.

2.
Braz. J. Pharm. Sci. (Online) ; 53(1): e16102, 2017. tab, graf
Article in English | LILACS, SES-SP, SESSP-IDPCPROD, SES-SP | ID: biblio-839466

ABSTRACT

ABSTRACT Membrane/lipid rafts (MLRs) are plasmalemmal microdomains that are essential for neuronal signaling and synaptic development/stabilization. Inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme-A reductase (statins) can disable the N-methyl-D-aspartate (NMDA) receptor through disruption of MLRs and, in turn, decrease NMDA-mediated anxiety. This hypothesis will contribute to understanding the critical roles of simvastatin in treating anxiety via the NMDA receptor.


Subject(s)
Animals , Male , Female , Rats , Anxiety/classification , Cholesterol/pharmacology , Simvastatin/administration & dosage , Anti-Anxiety Agents/pharmacology , N-Methylaspartate/agonists , Homeostasis , Anticholesteremic Agents
3.
Clin. biomed. res ; 35(1): 49-54, 2015. ilus
Article in English | LILACS | ID: lil-780276

ABSTRACT

Deficiency of guanidinoacetate methyltransferase, the first described creatine biosynthesis defect, leads to depletion of creatine and phosphocreatine, and accumulation of guanidinoacetate (GAA) in brain and body fluids. The present study aimed to investigate the influence of GAA on the activities of antioxidant enzymes, as well as on thiobarbituric acid-reactive substances (TBARS) and butyrylcholinesterase (BuChE) activity in the blood of rats. We also evaluated the effect of trolox (6-hydr oxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), GSH (glutathione) and L-NAME (NG-nitro-L-arginine methyl ester) on the alterations elicited by GAA. Methods: The rats were randomly divided into 8 groups: (1) control; (2) GAA (10, 30, 50, 100 mM/kg); (3) trolox (1 mM/kg) + control; (4) trolox (1 mM/kg) + GAA (100 mM/kg); (5) GSH (1 mM/kg) + control; (6) GSH (1 mM/kg) + GAA (100 mM/kg); (7) L-NAME (1 mM/kg) + control; (8) L-NAME + GAA (100 mM/kg). After the addition of compounds, erythrocytes and plasma were pre-incubated at 37°C for 1h and tested immediately. Results: GAA enhanced the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) in the erythrocytes and BuChE activity. In addition, GAA enhanced TBARS levels in the plasma. Trolox, GSH and L-NAME addition prevented the majority of alterations in oxidative stress parameters and the increase of BuChE activity that were caused by GAA. Data suggest that GAA alters antioxidant defenses and induces lipid peroxidation in the blood, as well altering BuChE activity. However, in the presence of trolox, GSH and L-NAME some of these alterations in oxidative stress and BuChE activity were prevented. Conclusions: Our findings lend support to a potential therapeutic strategy for this condition, which may include the use of appropriate antioxidants for ameliorating the damage caused by GAA...


Subject(s)
Animals , Rats , Antioxidants , Butyrylcholinesterase , Guanidinoacetate N-Methyltransferase , Oxidative Stress
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