Ilex paraguariensis supplementation may be an effective nutritional approach to modulate oxidative stress during perimenopause.

Perimenopause is a period in a woman's life that precedes menopause and is characterized by hormonal changes that result in increased oxidative stress. Since oxidative stress is associated with age-related diseases and perimenopausal symptoms including somato-vegetative manifestations, nutritional antioxidant supplementation may be an effective approach to minimizing this stress. Mate tea (MT) (Ilex paraguariensis), a typical and inexpensive beverage consumed in the Brazilian south-east, Argentina and Uruguay, increases antioxidant defense. We hypothesized that MT could minimize oxidative stress during perimenopause by modulating enzymatic antioxidant defense. To test this, we analyzed the lipid oxidative damage and antioxidant defense in erythrocytes and liver of rats, after MT treatment. Female Wistar rats (aged 16months) in proven perimenopause period received 20mg/kgBW/day of mate tea, by gavage (PM+MT group) or water (PM group). Female rats aged 4months (AD group) received water. Erythrocytes and liver were used to determine lipid oxidative damage, determined by malondialdehyde (MDA); superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) activities. Total plasma antioxidant capacity was examined by ferric reducing antioxidant power assay (FRAP) and estrogen by radioimmunoassay. MT increased FRAP and did not change estrogen levels. Increased SOD and GPx, and reduced MDA were observed in both tissues studied. Increased CAT activity was observed only in the liver. We confirmed the hypothesis that MT was capable of minimizing oxidative stress in this period of life by modulating antioxidant defense.

Short-term diabetes attenuates left ventricular dysfunction and mortality rates after myocardial infarction in rodents.

OBJECTIVES: To investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction. INTRODUCTION: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. METHODS: Male Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction. RESULTS: The myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23 ± 3%) when compared with the myocardial infarction (42 ± 7%, p < 0.001) animals at the final evaluation. The ejection fraction (22%, p = 0.003), velocity of circumferential fiber shortening (30%, p = 0.001), and left ventricular isovolumetric relaxation time (26%, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32 ± 3; diabetes + myocardial infarction: 35 ± 0.7; control-sham: 12 ± 2; myocardial infarction: 16 ± 0.1 pmol min⁻¹ mg⁻¹ protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5%) compared with the myocardial infarction animals (40.7%, p = 0.001). CONCLUSIONS: These data suggest that short-term hyperglycemia initiates compensatory mechanisms, as demonstrated by increased catalase levels, which culminate in improvements in the ventricular response, infarcted area, and mortality rate in diabetic rats exposed to ischemic injury.

Short-term diabetes attenuates left ventricular dysfunction and mortality rates after myocardial infarction in rodents

OBJECTIVES: To investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction. INTRODUCTION: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. METHODS: Male Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction. RESULTS: The myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23 ± 3 percent) when compared with the myocardial infarction (42 ± 7 percent, p<0.001) animals at the final evaluation. The ejection fraction (22 percent, p = 0.003), velocity of circumferential fiber shortening (30 percent, p = 0.001), and left ventricular isovolumetric relaxation time (26 percent, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32± 3; diabetes + myocardial infarction: 35± 0.7; control-sham: 12 ± 2; myocardial infarction: 16 ± 0.1 pmol min-1 mg-1 protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5 percent) compared with the myocardial infarction animals (40.7 percent, p = 0.001). CONCLUSIONS: These data suggest that short-term hyperglycemia initiates compensatory mechanisms, as demonstrated by increased catalase levels, which culminate in improvements in the ventricular response, infarcted area, and mortality rate in diabetic rats exposed to ischemic injury.

O papel do óxido nítrico na pressão anal esfincteriana de ratos submetidos à colite experimental / The role of nitric oxide in sphincteric anal pressure of rats with experimental colitis

O óxido nítrico (NO) é um radical livre sintetizado endogenamente por várias células do nosso organismo. Apresenta um amplo espectro de ações fisiológicas, sendo as mais importantes o seu mecanismo de ação parácrino no relaxamento da musculatura lisa, sua atividade neurotransmissora em vários sistemas e seu envolvimento no processo inflamatório. O NO é sintetizado em diferentes tecidos através da conversão da L-arginina em L-citrulina pela ação da enzima óxido nítrico sintase (NOS). OBJETIVOS: Este estudo tem por objetivo demonstrar o envolvimento do óxido nítrico no processo intestinal inflamatório de ratos Wistar submetidos à colite experimental com ácido acético. MATERIAL E MÉTODOS: Foram utilizados 20 ratos machos Wistar, com peso entre 250 e 350 gramas divididos em dois grupos de 10 animais. Os animais do grupo em estudo foram submetidos à administração intracolônica, por enema, de uma solução de ácido acético diluído a 7 por cento e com volume de 3 ml. O grupo controle recebeu apenas enema de solução salina. Foram avaliados os índices histológicos, a expressão da enzima óxido nítrico sintase (iNOS) e a pressão anal esfincteriana. RESULTADOS: Os índices histológicos apresentaram uma significativa elevação no grupo colite quando comparados ao grupo controle, tanto na avaliação macroscópica quanto na microscópica. A expressão da enzima iNOS também foi significativamente maior no grupo colite quando comparada ao grupo controle. A pressão anal esfincteriana foi significativamente mais baixa no grupo colite na comparação ao grupo controle. CONCLUSÃO: Os animais submetidos à colite experimental apresentam um aumento da expressão da enzima óxido nítrico sintase induzível (i-NOS). Este aumento, associado ao conseqüente aumento do nível de óxido nítrico, ocasiona uma diminuição dos níveis de pressão anal esfincteriana.

The nitric oxide (NO) is a free radical synthesized from some cells of our organism. It presents with an ample specter of physiological actions being the most important its mechanism of action in the relaxation of the smooth musculature, its neurotransmissor activity in some systems and its involvement in the inflammatory process. The NO is synthesized in different tissues by the conversion of the L-arginine in L-citruline with the action of the enzyme nitric oxide sintase(NOS). OBJECTIVES: the aim of this study is to demonstrate the involvement of nitric oxide in the inflammatory intestinal process of Wistar rats submitted to experimental colitis with ascetic acid. MATERIAL AND METHODS: 20 male Wistar rats had been used with weight between 250 and 350 g divided in two groups of 10 animals. The animals of the group in study had been submitted to intracolonic administration, by enema, of a solution with acid ascetic diluted to 7 percent - 3 ml. The control group received only enema with saline solution. The histological scores, the expression of the enzyme nitric oxide sintase (iNOS) and the sphincteric anal pressure had been evaluated. RESULTS: The histological scores had presented a significant rise in the group colitis when compared with the control group in the macroscopic as well as in the microscopical evaluation. The expression of the enzyme iNOS was also significantly higher in the colitis group when compared to the control group. The sphincteric anal pressure was significantly lower in the group colitis when compared to control group. CONCLUSION: The animals submitted to the experimental colitis presented an increase of the iNOS expression. This increase, associated with the consequent increase in nitric oxide level, causes a reduction of the sphincteric anal pressure levels.