Physical exercise and smoking are environmental factors that generally cause opposite health-promoting adaptations. Both physical exercise and smoking converge on mitochondrial adaptations in various tissues, including the pro-oxidant nervous system. Here, we analyzed the impact of cigarette smoking on exercise-induced brain mitochondrial adaptations in the hippocampus and pre-frontal cortex of adult mice. The animals were exposed to chronic cigarette smoke followed by 8 weeks of moderate-intensity physical exercise that increased mitochondrial activity in the hippocampus and pre-frontal cortex in the non-smoker mice. However, mice previously exposed to cigarette smoke did not present these exercise-induced mitochondrial adaptations. Our results suggest that smoking can inhibit some brain health-promoting changes induced by physical exercise.

No abstract

RESUMO Foram avaliados os efeitos tóxicos do hormônio 17β-estradiol (E2) livre e complexado à β-ciclodextrina (CD) sobre o comportamento e a fisiologia de tilápia (Oreochromis niloticus). Os peixes foram observados por 30 dias, em dois estágios do desenvolvimento (alevino e juvenil), pelo método ad libitum, para a confecção de um etograma. Posteriormente, juvenis foram divididos em três grupos: controle e expostos ao E2 (10ng/L) livre e complexado à β-ciclodextrina (β-CD:E2) por 90 dias. Foram avaliados o comportamento pelo método de varredura instantânea, o consumo de ração, o ganho de peso e a mortalidade em diferentes intervalos. Os alevinos e os juvenis apresentaram frequências de exibição comportamentais diferentes (P<0,05) nos eventos: Afastar (4,7±1,3 e 3,6±0,6%) e Ondulação de repulsão (2,3±0,9 e 1,3±1,0%). Os juvenis expostos ao complexo β-CD:E2 apresentaram aumento (P<0,05) na exibição dos comportamentos agressivos, como Afastar, Ataque caudal, Confronto prolongado, Perseguição, Fuga, e menor mortalidade, quando comparados ao grupo exposto ao E2 livre e controle. Pode-se concluir que a complexação do E2 com a β-CD alterou a toxicidade do E2, pois promoveu um aumento na frequência de exibição dos comportamentos agressivos e interferiu na mortalidade dos animais.

No abstract

In this study, the effects of exposure to rotenone on development were evaluated, particularly teratogenic and behavioral endpoints in the early life stages of zebrafish. This can serve as a model for Parkinson-like motor and non-motor symptoms, and anxiety-like behavior. The endpoints of percent epiboly, teratogenic effects, mortality, morphometry, thigmotaxis (TH), touch sensitivity (TS), and optomotor response (OMR) were analyzed in zebrafish embryo-larvae stage exposed to rotenone (5 to 20 µg/L). An increase in mortality of zebrafish was observed at 15 and 20 µg/L rotenone concentrations. The rotenone reduced the percent epiboly and increased the presence of teratogenic effects at concentrations of 10, 15, and 20 µg/L. Head and body size reductions were observed at all rotenone concentrations tested. Anxiety-like behaviors were observed with decreased displays of TH behavior in larvae exposed to 15 and 20 µg/L of rotenone. TS was reduced by 20 µg/L rotenone treatment. OMR and the eye diameter of zebrafish were not affected by rotenone exposure. Our results showed that rotenone has the potential to provoke non-motor symptoms, mainly anxiety-like behaviors, in the zebrafish's early life stages, making it a potential model for the study of Parkinson-like disease.