The effect of acute (120 mg/kg) and chronic (25 mg/kg, twice a day, for 4 days) intraperitonial injection of the nitric oxide (NO) synthase (NOS) inhibitor N G -nitro-L-arginine (L-NOARG) was evaluated on seizure induction by drugs such as pilocarpine and pentylenetetrazole (PTZ) and by sound stimulation of audiogenic seizure-resistant (R) and audiogenic seizure-susceptible (S) rats. Seizures were elicited by a subconvulsant dose of pilocarpine (100 mg/kg) only after NOS inhibition. NOS inhibition also simultaneously potentiated the severity of PTZ-induced limbic seizures (60 mg/kg) and protected against PTZ-induced tonic seizures (80 mg/kg). The audiogenic seizure susceptibility of S or R rats did not change after similar treatments. In conclusion, proconvulsant effects of NOS inhibition are suggested to occur in the pilocarpine model and in the limbic components of PTZinduced seizures, while an anticonvulsant role is suggested for the tonic seizures induced by higher doses of PTZ, revealing inhibitorspecific interactions with convulsant dose and also confirming the hypothesis that the effects of NOS inhibitors vary with the model of seizure.

Platinized carbon micro electrodes {-10 (tm diameter), positioned close {~ 5 urn) to the cell membrane of a human fibroblast, the ensemble constituting a semi-artificial synapse, are used to monitor events at the cellular level. A few tens of femlomoles of reactive oxygen species produced and emitted by the cell upon mechanical pricking with a glass micropipette (~ Î um diameter) are released into the liquid film of some hundred femtoliires comprised between the cytoplasmic membrane and the electrode surface, leading to a sudden and drastic rise in their concentrations {in the order of several micromoles). This oxidative stress-type response aims at disarming the aggressor and is thought to be shared by many {if not all) eukaryotic cells. This method allows to detect in real time and quantify the species constituting the oxidative burst cocktail: hydrogen peroxide, H2Oj, peroxynitrite, ON02, nitrogen monoxide, N0°, and nitrite, N02. They are likely to derive ultimately from superoxide anion, 02°, and nitrogen monoxide, NO*, synthesised by NADPH oxidase and NO synthase enzyme systems, respectively. By placing the mic reelect rode at different positions about the injured area of the cell membrane, it was concluded that the signals correspond to a spherical diffusion of the emitted electroactive species from a point-source.

This study investigated the repercussions of adjuvant-induced arthritis (AIA) on body composition and the structural organization of the soleus and cardiac muscles, including their vascularization, at different times of disease manifestation. Male rats were submitted to AIA induction by intradermal administration of 100 mL of Mycobacterium tuberculosis (50 mg/mL), in the right hind paw. Animals submitted to AIA were studied 4 (AIA4), 15 (AIA15), and 40 (AIA40) days after AIA induction as well as a control group of animals not submitted to AIA. Unlike the control animals, AIA animals did not gain body mass throughout the evolution of the disease. AIA reduced food consumption, but only on the 40th day after induction. In the soleus muscle, AIA reduced the wet mass in a time-dependent manner but increased the capillary density by the 15th day and the fiber density by both 15 and 40 days after induction. The diameter of the soleus fiber decreased from the 4th day after AIA induction as well as the capillary/fiber ratio, which was most evident on the 40th day. Moreover, AIA induced slight histopathological changes in the cardiac muscle that were more evident on the 15th day after induction. In conclusion, AIA-induced changes in body composition as well as in the soleus muscle fibers and vasculature have early onset but are more evident by the 15th day after induction. Moreover, the heart may be a target organ of AIA, although less sensitive than skeletal muscles.

Exercise-induced adaptations of the modulating mechanisms that influence the angiotensin (Ang II) responses assume different features depending on the venous bed. In femoral veins, exercise mobilizes vasodilator prostanoids to cooperate with NO in order to maintain reduced Ang II responses. On the other hand, exercise's influence on the Ang II responses in veins that drain blood from the mesenteric region has been poorly described. Therefore, the present study aimed to identify the effects of a single bout of exercise, as well as exercise training, on the Ang II responses in mesenteric veins. The present study also aimed to investigate the involvement of prostanoids, NO and ET-1 in eventual exercise-induced modifications in these veins. To this end, mesenteric veins taken from resting-sedentary, exercised-sedentary, resting-trained and exercised-trained animals were studied in organ baths. In addition, the mRNA expression of prepro-endothelin-1 (ppET-1), as well as that of the ET and ET receptors, were quantified by real-time PCR in these veins. The results show that, either in absence or in presence of L-NAME, the Ang II responses were not different between groups. In the presence of indomethacin, higher Ang II responses were observed in the resting-trained animals than in the resting-sedentary animals. This difference, however, disappeared when L-NAME, BQ-123 or BQ-788 were added during incubation. In addition, no differences in ppET-1, ET or ET mRNA expression were observed between groups. Furthermore, in the presence of PD123,319, the Ang II responses in the exercised-sedentary animals were higher than those in the resting-sedentary animals. In conclusion, exercise training mobilizes endothelin-1 (ET-1) to reinforce the Ang II-induced responses mainly through ET activation. On the other hand, vasodilator prostanoids are mobilized to act in parallel with NO in order to counterbalance the Ang II responses that have been potentiated by ET-1 in these trained animals.

The present study investigated the angiotensin II (Ang II) responses in rat femoral veins taken from 2-kidney-1clip (2K1C) hypertensive rats at 4 weeks after clipping, as well as the effects of exercise on these responses. In this manner, femoral veins taken from 2K1C rats kept at rest or exposed to acute exercise or to exercise training were challenged with Ang II or endothelin-1 (ET-1) in organ bath. Simultaneously, the presence of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were determined in these preparations by western blotting. In these experiments, femoral veins exhibited subdued Ang II responses. However, after nitric oxide (NO) synthesis blockade, the responses were higher in the femoral veins taken from animals kept at rest [0.137(0.049–0.245); n = 10] than those obtained in trained animals kept at rest [0.008(0.001–0.041); n = 10] or studied after a single bout of exercise [0.001(0.001–0.054); n = 11]. In preparations in which, in addition to NO synthesis, both the local production of prostanoids and the action of ET-1 on type A (ETA) or B (ETB) receptors were inhibited, the differences induced by exercise were no longer observed. In addition, neither ET-1 responses nor the presence of COX-1 and COX-2 in these preparations were modified by the employed exercise protocols. In conclusion, NO maintains Ang II responses reduced in femoral veins of 2K1C animals at rest. However, vasodilator prostanoids as well as other relaxing mechanisms, activated by ETB stimulation, are mobilized by exercise to cooperate with NO in order to maintain controlled Ang II responses in femoral veins.

O estresse oxidativo é definido como uma condição fisiopatológica em que produção de espécies reativas excede a capacidade das defesas antioxidantes do organismo em removê-las. Avaliar o grau de estresse oxidativo é essencial para a compreensão de diversos processos fisiologicos que mantêm a homestasia nasdiversas fases do ciclo da vida. Para isso, diversas técnicas simples e baratas podem ser empregadas. O presente trabalho propõe-se a apresentar algumas técnicas de estudo do estudo do estresse oxidativo, fazendo uma reflexão acerca de suas potencialidades e limitações. Pode se dizer que a credibilidade do estudo eleva--se pelo cuidado na padronização das técnicas, rigor do delineamento experimental e pela confirmação dos resultados através de diferentes técnicas, que avaliam diferentes processos que determinam o balanço redox.

Worldwide prevalence of noncommunicable chronic degenerative diseases is among the main causes of death worldwide. The consumption of some foods such as nuts and seeds may be beneficial in preventing these diseases. Dipteryx alata Vogel (DA), known popularly as Baru, belongs to the family Fabaceae and is a native fruit tree from the Brazilian savanna. The purpose of this study was to evaluate the use of seeds of DA on the metabolic and oxidative profile of Wistar rats. Animals were divided randomly into four groups (n = 10): G1 (control group), and G2 (treated with DA 20%), G3 (treated with DA 30%), and G4 (treated with DA 40%). After 40 days, animals were euthanized and metabolic and oxidative profiles were analyzed (glycemia, cholesterol, triglycerides [TGs], high-density lipoprotein-cholesterol [HDL-c], very low-density lipoprotein-cholesterol [VLDL-c], low-density lipoprotein-cholesterol [LDL-c], C reactive protein, aspartate aminotransferase, alanine aminotransferase, Lee index, weight, visceral fat, ferric reducing ability of plasma, and ferric-xylenol orange method. The use of the seeds was effective in reducing TGs, VLDL-c, LDL-c, and increasing HDL-c but did not interfere in the percentage of weight gain, visceral fat, levels of total cholesterol, and oxidative stress. Based on our results, it is possible to say that the use of DA may improve the lipid profile of Wistar rats and we may suggest that the consumption of DA almonds or products prepared with them may be an effective option for the intake of healthy products.

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