Nandrolone decanoate is prooxidant in the myocardium of exercised or sedentary rats / Decanoato de nandrolona é pro-oxidante no miocárdio de ratos treinados e sedentários / Decanoato de nandrolona es prooxidante en el miocardio de ratones entrenados y sedentarios

ABSTRACT Introduction: Nandrolone decanoate is a synthetic testosterone analogue considered one of the most widely used anabolic androgenic steroids (AAS) among adolescents and athletes. Chronic ingestion of AAS increases the incidence of cardiovascular abnormalities in athletes, but the mechanism that causes these changes remains unknown. Objectives: The purpose of this study is to verify the possible effects of the use of anabolic androgenic steroids (AAS) on the morphology and oxidative metabolism of the heart in exercised and sedentary rats. Methods: This is a comparative prospective level II study. Twenty-four Wistar rats were distributed in groups that performed voluntary (TG) and sedentary (SG) running exercises, and used AAS: the Anabolic Training Group (ATG), and the Anabolic Sedentary Group (ASG). During the three months of the running protocol, the animals received an intramuscular injection of 5 mg/kg b.p. of AAS. After the training period, the rats were euthanized and the hearts were removed for evaluation of lipid peroxidation and antioxidant capacity, and for morphometric analysis. Results: The anabolic groups, ASG (0.3072 ± 0.0531) and ATG (0.2732 ± 0.0413), presented higher lipid peroxidation when compared to the non-anabolic groups SG (0.1705 ± 0.0224) and TG (0.1785 ± 0.0340). Conclusion: There was no change in total antioxidant capacity or in the thickness of the interventricular septum and left ventricular wall. Thus, the use of anabolic androgenic steroids did not cause morphological changes in the myocardium. However it did alter the oxidative metabolism. It was also verified that aerobic exercise had no protective effect against lipid peroxidation in the myocardium caused by the use of AAS. Level of evidence II; Prospective comparative study.

RESUMO Introdução: O decanoato de nandrolona é um análogo sintético da testosterona, considerado um dos esteroides anabólicos androgênicos (EAA) mais utilizados entre adolescentes e atletas. Sua ingestão crônica aumenta a incidência de anormalidades cardiovasculares em atletas, porém o mecanismo que causa essas alterações ainda permanece desconhecido. Objetivos: O estudo teve como objetivo verificar os possíveis efeitos do uso de esteroides anabólicos androgênicos (EAA) na morfologia e no metabolismo oxidativo do coração de ratos treinados e sedentários. Métodos: Trata-se de um estudo prospectivo comparativo nível II. Vinte e quatro ratos Wistar foram distribuídos em grupos que realizaram exercícios de corrida voluntária (GT) e sedentários (GS) e faziam uso dos EAA, Grupo Treinado com Anabolizante (GTA) e Grupo Sedentário com Anabolizante (GSA). Durante os três meses do protocolo de corrida, os animais receberam injeção intramuscular de 5 mg/kg p.c. de EAA. Após o período de treinamento, houve a eutanásia e remoção do coração dos ratos para avaliação da peroxidação lipídica e capacidade antioxidante, além da análise morfométrica. Resultados: Verificaram-se que os grupos anabolizantes, GSA (0,3072 ± 0,0531) e GTA (0,2732 ± 0,0413), apresentaram maior peroxidação lipídica quando comparados aos grupos não anabolizantes GS (0,1705 ± 0,0224) e GT (0,1785 ± 0,0340). Conclusões: Não houve alteração na capacidade antioxidante total, assim como não houve alteração na espessura do septo interventricular e da parede ventricular esquerda. Portanto, o uso de esteroides anabólicos androgênicos não provocou alterações morfológicas no miocárdio, contudo alterou o metabolismo oxidativo. Verificou-se também que a prática de exercício aeróbico não teve efeito protetor contra a peroxidação lipídica no miocárdio provocada pelo uso dos EAA. Nível de evidência II; Estudo prospectivo comparativo.

RESUMEN Introducción: El decanoato de nandrolona es un análogo sintético de la testosterona considerado uno de los esteroides anabólicos androgénicos (EAA) más utilizados entre los adolescentes y atletas. Su ingestión crónica aumenta la incidencia de anomalías cardiovasculares en atletas, aunque el mecanismo que causa esas alteraciones sigue siendo desconocido. Objetivos: El estudio tuvo como objetivo verificar los posibles efectos del uso de esteroides anabólicos androgénicos (EAA) en la morfología y en el metabolismo oxidativo del corazón de ratones entrenados y sedentarios. Métodos: Se trata de un estudio prospectivo comparativo nivel II. Fueron distribuidos 24 ratones Wistar en grupos que realizaron ejercicios de carrera voluntaria (GE) y sedentarios (GS), y hacían uso de los EAA, Grupo Entrenado con Anabolizante (GEA) y Grupo Sedentario con Anabolizante (GSA). Durante los tres meses del protocolo de carrera, los animales recibieron inyección intramuscular de 5 mg/kg p.c. de EAA. Después del período de entrenamiento, hubo la eutanasia y remoción del corazón de los ratones, para evaluación de la peroxidación lipídica y capacidad antioxidante, además del análisis morfométrico. Resultados: Se verificó que los grupos anabolizantes, GSA (0,3072 ± 0,0531) y GEA (0,2732 ± 0,0413), presentaron mayor peroxidación lipídica cuando comparados a los grupos no anabolizantes GS (0,1705 ± 0,0224) y GE (0,1785 ± 0,0340). Conclusiones: No hubo alteración en la capacidad antioxidante total, así como no hubo alteración en el espesor del septo interventricular y de la pared ventricular izquierda. Por lo tanto, el uso de esteroides anabólicos androgénicos no provocó alteraciones morfológicas en el miocardio, aunque alteró el metabolismo oxidativo. Se verificó también que la práctica de ejercicio aeróbico no tuvo efecto protector contra la peroxidación lipídica en el miocardio provocada por el uso de EAA. Nivel de evidencia II; Estudio prospectivo comparativo.

Lateral parabrachial afferent areas and serotonin mechanisms activated by volume expansion.

Recent evidence has shown that the serotonergic mechanism of the lateral parabrachial nucleus (LPBN) participates in the regulation of renal and hormonal responses to isotonic blood volume expansion (BVE). We investigated the BVE-induced Fos activation along forebrain and hindbrain nuclei and particularly within the serotonergic clusters of the raphé system that directly project to the LPBN. We also examined whether there are changes in the concentration of serotonin (5HT) within the raphé nucleus in response to the same stimulus. With this purpose, we analyzed the cells doubly labeled for Fos and Fluorogold (FG) following BVE (NaCl 0.15 M, 2 ml/100 g b.w., 1 min) 7 days after FG injection into the LPBN. Compared with the control group, blood volume-expanded rats showed a significant greater number of Fos-FG double-labeled cells along the nucleus of the solitary tract, locus coeruleus, hypothalamic paraventricular nucleus, central extended amygdala complex, and dorsal raphé nucleus (DRN) cells. Our study also showed an increase in the number of serotonergic DRN neurons activated in response to isotonic BVE. We also observed decreased levels of 5HT and its metabolite 5-hydroxyindoleacetic acid (measured by high-pressure liquid chromatography) within the raphé nucleus 15 min after BVE. Given our previous evidence on the role of the serotonergic system in the LPBN after BVE, the present morphofunctional findings suggest the existence of a key pathway (DRN-LPBN) that may control BVE response through the modulation of 5HT release.

Estradiol reduces cumulative mercury and associated disturbances in the hypothalamus-pituitary axis of ovariectomized rats.

The aim of this research was to verify the incidence of endocrine dysfunction associated with mercury intoxication in the hypothalamus-pituitary reproductive system of normally cycling or castrated female rats and the possible protective action of estrogen replacement therapy. We found no differences in the frequency of estrus cycle stages (diestrus I, diestrus II, proestrus, and estrus) in normally cycling female rats during 54 days of daily oral administration of 0.004, 0.02, and 1 mg/kg MeHgCl. Conversely, the higher dose (1 mg/kg) induced a significant decrease in content of luteinizing hormone releasing hormone (LHRH) into the medial hypothalamus when administered daily during 3 days in ovariectomized rats. This effect was associated with increased levels of mercury found in the anterior pituitary gland and medial hypothalamus, rather than the anterior and posterior hypothalamus, striatum or cerebellum. A decrease in plasma levels of luteinizing hormone (LH) was also detected after administration of 7.5 mg/kg MeHgCl. These disturbances in LHRH and LH secretion induced by mercury were abolished or superimposed (respectively) by estrogenic replacement therapy (0.025 mg/kg 17beta estradiol cypionate, intramuscular). These effects were associated with a significant reduction in mercury content of the anterior pituitary gland and medial hypothalamus, suggesting a protective estrogenic effect.