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This study investigated the pathological morphofunctional adaptations related to the imbalance of exercise tolerance triggered by paraquat (PQ) exposure in rats. The rats were randomized into four groups with eight animals each: (a) SAL (control): 0.5 ml of 0.9% NaCl solution; (b) PQ10: PQ 10 mg/kg; (c) PQ20: PQ 20 mg/kg; and (d) PQ30: PQ 30 mg/kg. Each group received a single injection of PQ. After 72 hours, the animals were subjected to an incremental aerobic running test until fatigue in order to determine exercise tolerance, blood glucose and lactate levels. After the next 24 h, lung, liver and skeletal muscle were collected for biometric, biochemical and morphological analyses. The animals exposed to PQ exhibited a significant anticipation of anaerobic metabolism during the incremental aerobic running test, a reduction in exercise tolerance and blood glucose levels as well as increased blood lactate levels during exercise compared to control animals. PQ exposure increased serum transaminase levels and reduced the glycogen contents in liver tissue and skeletal muscles. In the lung, the liver and the skeletal muscle, PQ exposure also increased the contents of malondialdehyde, protein carbonyl, 8-hydroxy-2'-deoxyguanosine, superoxide dismutase and catalase, as well as a structural remodelling compared to the control group. All these changes were dose-dependent. Reduced exercise tolerance after PQ exposure was potentially influenced by pathological remodelling of multiple organs, in which glycogen depletion in the liver and skeletal muscle and the imbalance of glucose metabolism coexist with the induction of lipid, protein and DNA oxidation, a destructive process not counteracted by the upregulation of endogenous antioxidant enzymes.

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Rev Neurocienc 2012;20(1):68-72 original 68 RESUMO Objetivo. Verificar possíveis alterações quantitativas de corpos de neurônios, no córtex cerebral, causadas pelo uso de esteróides anabolizantes. Método. Foram utilizados trinta camundongos divididos em 3 grupos (grupo 1 -Deca Durabolin®; grupo 2-Potenay®; grupo 3-Salina) tratados uma vez na semana e submetidos à natação três vezes na semana, tendo o tratamento a duração total de um mês. Após a eutanásia os encéfalos foram retirados e foram preparados segundo técnica histológica convencional e corados com violeta cresil, através da análise morfométrica foram buscados os dados comparativos. Resultados. Os resultados obtidos revelaram que houve uma diminuição significativa do número de corpos de neurônios nos animais tratados (P<0,01) quando comparados com o grupo controle, porém não foi significativo (P>0,05) quando comparados os dois sexos. Os animais do grupo Potenay® apresentaram 23,36 corpos de neurônios enquanto que os animais do grupo Deca-durabolin® apresentaram 23,40 corpos de neurônios, os valores médios de corpos de neurônios foram iguais e inferiores aos observados para o grupo controle que foi de 31,70. Conclusão. Concluímos que a densidade de corpos de neurônios no córtex cerebral mostra uma diminuição significativa nos camundongos submetidos ao tratamento com esteróides anabolizantes em relação ao grupo controle. ABSTRACTObjective. Investigate quantitative changes in cerebral cortex neurons bodies caused by the use of anabolic steroids. Method. Thirty mice were used, which received treatment with steroids (group 1-Deca Durabolin®; group 2-Potenay®; group 3-Saline) once a week and submitted to swimming three times a week, taking total treatment duration one month. After euthanasia, the brains were removed, fixed and histological processed and cresyl violet was used for staining. The slices were analyzed by light microscope and software to count the neurons bodies. Results. The results shows that there was a significant decrease of neurons bodies number in treated groups (P<0.01) when compared with the control group, but was not significant (P>0.05) when both genders were compared. In Potenay ® group, the animals showed 23.36 neurons bodies while the animals in Deca-durabolin® group had 23.40. The average values of neuron bodies were equal and lower than of control group, which was 31.70. Conclusion. The neuronal bodies density in cerebral cortex decreased significantly in mice undergoing treatment with steroids in relation to control group. Original Recebido em: 15/03/11 Aceito em: 09/08/11 Conflito de interesses: não Suporte financeiro: Fapemig. Trabalho realizado no Departamento de Anatomia da Universidade Federal de Alfenas, Alfenas-MG, Brasil. 1.Biomédico graduando pela Unifal-MG, Alfenas-MG, Brasil. 2.Biólogo graduando pela Unifal-MG, Alfenas-MG, Brasil. 3.Zootecnista, Doutor e Docente da Unifal-MG, Alfenas-MG, Brasil. 4.Cirurgião dentista, Doutor Docente da Unifal-MG, Alfenas-MG, Brasil. 5.Médico, Doutor Docente da Unifal-MG, Alfenas-MG, Brasil....

Functional food intake has been highlighted as a strategy for the prevention of cardiovascular diseases by reducing risk factors. In this study, we compared the effects of oral treatment with soy milk and simvastatin on dyslipidemia, left ventricle remodeling and atherosclerotic lesion of LDL receptor knockout mice (LDLr-/-) fed a hyperlipidic diet. Forty 3-month old male LDLr-/- mice were distributed into four groups: control group (C), in which animals received standard diet; HL group, in which animals were fed a hyperlipidic diet; HL+SM or HL+S groups, in which animals were submitted to a hyperlipidic diet plus soy milk or simvastatin, respectively. After 60 days, both soy milk and simvastatin treatment prevented dyslipidemia, atherosclerotic lesion progression and left ventricle hypertrophy in LDLr-/- mice. These beneficial effects of soy milk and simvastatin were associated with reduced oxidative stress and inflammatory state in the heart and aorta caused by the hyperlipidic diet. Treatment with soy milk was more effective in preventing HDLc reduction and triacylglycerol and VLDLc increase. On the other hand, simvastatin was more effective in preventing an increase in total cholesterol, LDLc and superoxide production in aorta, as well as CD40L both in aorta and left ventricle of LDLr-/-. In conclusion, our results suggest a cardioprotective effect of soy milk in LDLr-/- mice comparable to the well-known effects of simvastatin.