Crotoxin-induced behavioral effects in rats

Crotoxin is the major component of Crotalus durissus terrificus venom. In view of the presence of high-affinity specific binding sites for crotoxin in the brain, the objective of this work was to investigate whether crotoxin induces behavioral effects in the open-field and hole-board tests. Adult male Wistar rats (180-220 g) treated with crotoxin, 100, 250 and 500 mu g/kg, ip, administered 2 h before the test, presented statistically significant behavioral alterations (ANOVA for one-way classification complemented with Dunnet test, P<0.05). In the open-field test, 250 and 500 mu g/kg of crotoxin increased freezing (from 3.22 sec to 10.75 sec and 11.2 sec) and grooming (from 13.44 sec to 22.75 sec and 21.22 sec) and decreased ambulation (from 64.8 to 39.38 and 45.8). The dose of 500 mu g/kg also decreased rearing (from 24.9 to 17.5). In the hole-board test, 500 mu g/kg of crotoxin decreased head-dip count (from 6.33 to 4.00). All the crotoxin-induced behavioral effects were antagonized by an anxiolytic dose of diazepam (1.5 mg/kg, ip, 30 min before the tests). These results show that crotoxin reduced open-field activity and exploratory behavior as well. We suggest that these effects express an increased emotional state induced by this toxin.

Effects of a leucine-rich diet on body composition during nutritional recovery in rats

OBJECTIVE: Protein malnutrition is characterized by a number of morphologic and physiologic alterations, including intestinal mucosal atrophy and impaired nutrient absorption. Impaired absorption accentuates nutritional deficiency and accelerates body weight loss and changes in body chemistry. Because leucine is a ketogenic and oxidative amino acid and stimulates the protein synthesis, we examined the ability of young rats to recover from protein malnutrition by feeding them a control balanced or a leucine-rich diet for 60 d.METHODS: At the end of the 60-d period, body, liver, and muscle weights; glucose, methionine, and leucine intestinal absorption; and carcass chemical composition were evaluated.RESULTS: Body weight gain was higher in the control balanced and leucine-rich groups than in control rats, indicating that adequate refeeding allows body weight to recover in these groups. Methionine and glucose absorptions were impaired in malnourished rats but were restored after nutritional recovery. The leucine-rich diet resulted in an increase in carcass collagen nitrogen but maintained the carcass structural nitrogen.CONCLUSIONS: These results indicated that leucine supplementation during nutritional recovery from protein malnutrition improves protein carcass restoration. However, the precise mechanism of the leucine effects involved in this response remains to be elucidated.

Low triioothyronine (T-3) or reverse triioothyronine (rT(3)) syndrome modifies gene expression in rats with congestive heart failure

Heart failure (NF) is frequently associated with euthyroid sicksyndrome (low T-3 and elevated rT(3)). We investigated if altered thyroid hormone in HF could affect expression of the TH receptor (TR alpha 1), and alpha and beta myosin heavy chains (alpha-MHC beta-MHC). HF was provoked in rats by aortic stenosis. We showed that rT(3) generated front liver and kidney deiodination significantly increased and T-3 decreased in HE; there was significantly higher TR alpha 1 expression, no alpha-MHC expression, but beta-MHC expression. Changes in TR alpha 1 could be compensating for low T-3 from HF.

Arterial-hypertension in the elderly

The authors review the epidemiology, the etiological factors, the effect of the treatment in the evolution of the cardiovascular disease in arterial hypertension in elderly, and the use of angiotensin-converting-enzyme inhibitors such as a treatment option.

EARLY ACTIVATION OF SPLENIC MACROPHAGES BY TUMOR-NECROSIS-FACTOR-ALPHA IS IMPORTANT IN DETERMINING THE OUTCOME OF EXPERIMENTAL HISTOPLASMOSIS IN MICE

Experimental infection of animals with Histoplasma capsulatum caused a massive macrophage infiltration into the spleen and induced the production of tumor necrosis factor alpha (TNF-alpha) locally. The cytokine was also produced in vitro by peritoneal exudate macrophages exposed to a large inoculum of yeast cells. Depletion of the cytokine by injection of polyclonal sheep anti-TNF-alpha antibody was detrimental to sublethally infected mice. Fungous burdens in the spleens of TNF-alpha-depleted mice were higher than they were in the infected control mice at days 2, 7, and 9 after infection, and the antibody-treated animals succumbed to the infection. Histopathological study of spleen sections revealed that splenic macrophages were not able to control proliferation of intracellular yeasts as a result of TNF-alpha depletion. It seems that TNF-alpha plays a role in early activation of splenic macrophages which is important in controlling the outcome of an infection.