Effects of aquatic exercise on mental health, functional autonomy and oxidative stress in depressed elderly individuals: A randomized clinical trial

OBJECTIVES: The aim of this study was to investigate the effects of aquatic exercise on mental health, functional autonomy and oxidative stress parameters in depressed elderly individuals. METHODS: Initially, ninety-two elderly individuals were included in the study and were allocated into the depression group (n=16) and nondepression group (n=14). Both groups engaged in the aquatic exercise program for 12 weeks, including two weekly sessions (45 min/session) at a low intensity (between 50% and 60% of maximal heart rate or Borg scale scores of 13 to 14) throughout the intervention. All outcomes were evaluated at baseline and 12 weeks later. RESULTS: The patients were 63.5±8.8 years old. The following scores were decreased after training in the depressed group: depression (53%), anxiety (48%), and Timed Up & Go (33%). The following scores increased: Berg Balance Scale (9%) and flexibility (44%). Regarding the blood-based parameters, there were decreases in protein carbonylation (46%) and nitric oxide (60%) and increases in glutathione (170%) and superoxide dismutase (160%) in the depression group (po0.005). CONCLUSIONS: The aquatic exercise program reduces depression and anxiety, improves functional autonomy and decreases oxidative stress in depressed elderly individuals

Cigarette smoke exposure induces ROS-mediated autophagy by regulating sestrin, AMPK, and mTOR level in mice

Many pathological conditions linked to cigarette smoking are caused by the production of reactive oxygen species (ROS). The present study was conducted to analyze the effect of ROS on the lungs of Swiss mice exposed to cigarette smoking, focusing on autophagy-mediated mechanisms, and investigate the involvement of SESN2, AMPK, and mTOR signaling. Mice were exposed to cigarette smoke (CS) for 7, 15, 30, 45, and 60 days; the control group was not exposed to CS. Only mice exposed to CS for 45 days were selected for subsequent N-acetylcysteine (NAC) supplementation and smoke cessation analyses. Exposure to CS increased the production of ROS and induced molecular changes in the autophagy pathway, including an increase in phosphorylated AMPK and ULK1, reduction in phosphorylated mTOR, and increases in SESN2, ATG12, and LC3B levels. NAC supplementation reduced ROS levels and reversed all molecular changes observed upon CS treatment, suggesting the involvement of oxidative stress in inducing autophagy upon CS exposure. When exposure to CS was stopped, there were decreases in the levels of oxidative stress, AMPK and ULK1 phosphorylation, and autophagy-initiating molecules and increase in mTOR phosphorylation. In conclusion, these results suggest the involvement of ROS, SESN2, AMPK, and mTOR in the CS-induced autophagic process in the lung

Effects of diet-induced hypercholesterolemia and gold nanoparticles treatment on peripheral tissues

Cholesterol is a lipid molecule of great biological importance to animal cells. Dysregulation of cholesterol metabolism leads to raised blood total cholesterol levels, a clinical condition called hypercholesterolemia. Evidence has shown that hypercholesterolemia is associated with the development of liver and heart disease. One of the mechanisms underlying heart and liver alterations induced by hypercholesterolemia is oxidative stress. In this regard, in several experimental studies, gold nanoparticles (AuNP) displayed antioxidant properties. We hypothesized that hypercholesterolemia causes redox system imbalance in the liver and cardiac tissues, and AuNP treatment could ameliorate it. Young adult male Swiss mice fed a regular rodent diet or a high cholesterol diet for eight weeks and concomitantly treated with AuNP (2.5 μg/kg) or vehicle by oral gavage. Hypercholesterolemia increased the nitrite concentration and glutathione (GSH) levels and decreased the liver’s superoxide dismutase (SOD) activity. Also, hypercholesterolemia significantly enhanced the reactive oxygen species (ROS) and GSH levels in cardiac tissue. Notably, AuNP promoted the redox system homeostasis, increasing the SOD activity in hepatic tissue and reducing ROS levels in cardiac tissue. Overall, our data showed that hypercholesterolemia triggered oxidative stress in mice’s liver and heart, which was partially prevented by AuNP treatment

Resumos concluídos - Nanomateriais

Resumos concluídos - Nanomateriai

Resumos em andamento - Neurociências

Resumos em andamento - Neurociência

Resumos em andamento - Neurociências

Resumos em andamento - Neurociência

Resumos em andamento - Bioquímica

Resumos em andamento - Bioquímic