Qualidade seminal e perfil metabólico de caprinos alimentados com semente de linhaça na dieta / Semen quality and metabolic profile of goats fed flaxseed in the diet

O objetivo da presente pesquisa foi avaliar o efeito da inclusão de semente de linhaça na dieta sobre a qualidade seminal e o perfil metabólico de machos caprinos. Foram utilizados 16 machos da raça Saanen, distribuídos aleatoriamente em quatro grupos, recebendo níveis de inclusão de semente de linhaça (0, 4, 8 e 12%) na dieta, durante um período de 60 dias. As coletas e as avaliações seminais foram realizadas duas vezes por semana. Os animais foram submetidos a coletas quinzenais de sangue, durante todo o período experimental. Os dados foram avaliados por ANOVA e pela análise de regressão a 5% de significância. Houve comportamento cúbico para motilidade espermática progressiva, que apresentou o maior valor (82,30%) com a adição de 9,92% de semente de linhaça na dieta (P<0,05). Houve comportamento cúbico para concentração plasmática de triglicerídeos, e o nível de 8% de semente de linhaça na dieta apresentou média de 43,32mg dL-1, acima dos valores normais para a espécie caprina (P<0,05). A inclusão de semente de linhaça na dieta de machos caprinos proporcionou melhora na produção espermática e na qualidade seminal. No entanto, devem-se considerar os possíveis efeitos dos níveis superiores a 4% de semente de linhaça sobre o perfil metabólico dos animais.(AU)

This study aimed to evaluate the effect of flaxseed inclusion in the diet of male goats through the semen quality and metabolic profile. Randomly allocated 16 Saanen males were placed into four groups receiving flaxseed inclusion levels (0, 4, 8 and 12%) in the diet over a period of 60 days. The collections and seminal evaluations were performed twice a week. The animals were subjected to biweekly blood collections from the beginning to the end of the trial period. The data were evaluated by ANOVA and regression analysis at 5% significance. A cubic behavior for motility, with the highest value (82.30%) with the addition of 9.92% of flaxseed in the diet (P< 0.05) was detected. A cubic behavior for plasma triglyceride concentration and the level of 8% of flaxseed in the diet averaged 43.32mg dL -1 above normal values for goats (P< 0.05) was detected. The inclusion of flaxseed in the diet of male goats improved sperm production and quality. However, one should consider the possible effects of the levels above 4% of flaxseed on the metabolic profile of the animals.(AU)

Gadolinium increases the vascular reactivity of rat aortic rings

Gadolinium (Gd) blocks intra- and extracellular ATP hydrolysis. We determined whether Gd affects vascular reactivity to contractile responses to phenylephrine (PHE) by blocking aortic ectonucleoside triphosphate diphosphohydrolase (E-NTPDase). Wistar rats of both sexes (260-300 g, 23 females, 7 males) were used. Experiments were performed before and after incubation of aortic rings with 3 µM Gd. Concentration-response curves to PHE (0.1 nM to 0.1 mM) were obtained in the presence and absence of endothelium, after incubation with 100 µM L-NAME, 10 µM losartan, or 10 µM enalaprilat. Gd significantly increased the maximum response (control: 72.3 ± 3.5; Gd: 101.3 ± 6.4 percent) and sensitivity (control: 6.6 ± 0.1; Gd: 10.5 ± 2.8 percent) to PHE. To investigate the blockade of E-NTDase activity by Gd, we added 1 mM ATP to the bath. ATP reduced smooth muscle tension and Gd increased its relaxing effect (control: -33.5 ± 4.1; Gd: -47.4 ± 4.1 percent). Endothelial damage abolished the effect of Gd on the contractile responses to PHE (control: 132.6 ± 8.6; Gd: 122.4 ± 7.1 percent). L-NAME + Gd in the presence of endothelium reduced PHE contractile responses (control/L-NAME: 151.1 ± 28.8; L-NAME + Gd: 67.9 ± 19 percent AUC). ATP hydrolysis was reduced after Gd administration, which led to ATP accumulation in the nutrient solution and reduced ADP concentration, while adenosine levels remained the same. Incubation with Gd plus losartan and enalaprilat eliminated the pressor effects of Gd. Gd increased vascular reactivity to PHE regardless of the reduction of E-NTPDase activity and adenosine production. Moreover, the increased reactivity to PHE promoted by Gd was endothelium-dependent, reducing NO bioavailability and involving an increased stimulation of angiotensin-converting enzyme and angiotensin II AT1 receptors.

Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity

This review addresses the mechanisms of methylmercury (MeHg)-induced neurotoxicity, specifically examining the role of oxidative stress in mediating neuronal damage. A number of critical findings point to a central role for astrocytes in mediating MeHg-induced neurotoxicity as evidenced by the following observations: a) MeHg preferentially accumulates in astrocytes; b) MeHg specifically inhibits glutamate uptake in astrocytes; c) neuronal dysfunction is secondary to disturbances in astrocytes. The generation of reactive oxygen species (ROS) by MeHg has been observed in various experimental paradigms. For example, MeHg enhances ROS formation both in vivo (rodent cerebellum) and in vitro (isolated rat brain synaptosomes), as well as in neuronal and mixed reaggregating cell cultures. Antioxidants, including selenocompounds, can rescue astrocytes from MeHg-induced cytotoxicity by reducing ROS formation. We emphasize that oxidative stress plays a significant role in mediating MeHg-induced neurotoxic damage with active involvement of the mitochondria in this process. Furthermore, we provide a mechanistic overview on oxidative stress induced by MeHg that is triggered by a series of molecular events such as activation of various kinases, stress proteins and other immediate early genes culminating in cell damage.

Effect of inhibitory avoidance training on [3H]-glutamate binding in the hippocampus and parietal cortex of rats

Glutamate receptors have been implicated in memory formation. The aim of the present study was to determine the effect of inhibitory avoidance training on specific [3H]-glutamate binding to membranes obtained from the hippocampus or parietal cortex of rats. Adult male Wistar rats were trained (0.5-mA footshock) in a step-down inhibitory avoidance task and were sacrificed 0, 5, 15 or 60 min after training. Hippocampus and parietal cortex were dissected and membranes were prepared and incubated with 350 nM [3H]-glutamate (N = 4-6 per group). Inhibitory avoidance training induced a 29 percent increase in glutamate binding in hippocampal membranes obtained from rats sacrificed at 5 min (P<0.01), but not at 0, 15, or 60 min after training, and did not affect glutamate binding in membranes obtained from the parietal cortex. These results are consistent with previous evidence for the involvement of glutamatergic synaptic modification in the hippocampus in the early steps of memory formation

Effects of methylmercury exposure during the second stage of rapid postnatal brain growth on negative geotaxis and on delta-aminolevulinate dehydratase of suckling rats

In the present study, we examined the effects of exposure to methylmercury (0, 2.3, 4.6, 6.9 and 9.2 mg/kg, daily for 5 consecutive days, sc) during the second stage of rapid postnatal brain development (8 to 12 days of age) on the sulfhydryl-containing enzyme delta-aminolevulinate dehydratase (ALA-D, E.C. 4.2.1.24) from brain, liver and kidney and on motor performance (latency to complete a negative geotaxis response) of rats. ALA-D specific activity of 13-day old rats of both sexes (7-12 per group) was reduced significantly in rats treated with 6.9 mg/kg and 9.2 mg/kg in brain (about 40 per cent , P < 0.05) and in liver (about 25 per cent , P < 0.05). Renal ALA-D specific activity was not affected by methylmercury treatment. The in vitro IC50 for inhibition of brain, liver and renal ALA-D was 79.3, 81.8 and 39.1 microM, respectively. The latency to complete the negative geotaxis response of 12-day old rats was increased by 6.9 (7.9 +/- 0.7 s, mean +/- SEM) and 9.2 mg/kg methylmercury (7.8 +/- 0.5 s) when compared with control rats (5.8 +/- 0.3 s), suggesting an impairment in motor performance of exposed rats. These results demonstrate that exposure to relatively high doses of methylmercury during the second stage of brain development causes a significant reduction in brain and hepatic ALA-D. The absence of inhibition of ALA-D by lower doses may be related to the relatively low in vitro sensitivity of the enzyme to methylmercury. The possible involvement of ALA-D inhibition on the neurotoxicity of methylmercury deserves additional investigation

Effects of undernutrition during suckling on foot-shock escape behavior and of post-traini9ng beta-endorphin administration on inhibitory avoidance task test behavior of young rats

The hypothalamic beta-endorphin system of young Wistar rats of both sexes (21-day-old) responds in a distinct way to behavioral situations when compared to adult rats (90 to 120-day-old). In the present study we investigated whether the post-training amnestic effect of beta-endorphin previously demonstrated in Wistar adult rats is also observed young (21-day-old) well-nourished and undernourished rats. rats were undernourished since birth by feeding their dams an 8% casein diet, while well-nourished off spring were fed by dams maintained on a 20% caseindiet beta-endorphin was administered after training in a step-down inhibitory avoidance task using a 0.2 or 0.8 m-A footshock. Retention was tested 24 h later. We observed that the dose of beta-endorphin (1 ug/kg, ip) previously reported to have an amnestic effect on adult rats was ineffective in weanling rats of both nutritional groups. At a higher dose (2 ug/kg, ip) and using a 0.2-mA shock, beta-endorphin impaired the retention only of well-nourished rats. Test-to training difference (in s) in step-down latency for well-nourished beta-endorphin-treated rats was 7 vs 25 s for well-nourished rats treated with saline (P<0.05). Undernourished rats were hyperreactive to this shock intensity. Footshock escape latency (in s) for undernourished rats was 3.56 vs 5.80 for well-nourished rats (P<0.05, experiment 1) and 5.01 vs 10.89 (P<0.05 in experiment 2) and showed better retenmtion than did well-nourished rats. Test-totraining step down latency (in s) for saline-treated undernourished rats was abouth 108 vs 28 saline-treated well-nourished rats (P<0.05). At 0.8-m-A, neither beta-endorphin nor undernutrition affected performance. These resultssuggest that well-nourished rats respons in a distinct way to post-training beta-enmdorphin when compared to adult rats of both sexes. The absence of amnesia in weanling undernourished rats may be related to the enhacenced sensitivity of both sexes. The absence of amnesia in weanling undernourished rats may be related to the enhanced sensitivity of these animals to a 0.2-mA footshock

Synaptosomal apyrase in the hypiothalamus of adult rats

1. The synaptosomal fraction isolated from hypothalamus of adult rats on sucrose density gradient hydrolyzes the labile phosphatase from ATP and ADP, thereby satisfying the general definition of apyrase activity. 2. The parallel behavior of ATPase and ADPase activities under different reaction conditions suggests the presence of a "true" apyrase enzyme. The optimum conditions for the are the same for both nucleotides: pH 8.0, 0.6 mM nucleotide and 1.5 mM cation. At temperatures between 10 and 40-C, both activities increase with no change in the ATP/ADP hydrolysis ratio. Thermal inactivation or inhibition of the enzyme activity by iodoacetamide, p-hydroxynercuribenzoate or 2- mercaptoethanol affected the hydrolysis of both substrates in a similar manner. 3- Adenylate Kinase and phyrophosphatase activities were not detected in the preparation. 4. The enzyme is located on the outer surface of the synaptosomal membrane: intact and lysed synaptosomes have similar activity and the supernatant obtained by centrifugation of intact synaptosomal preparations does not hydrolyze ATP or ADP

Effects of undernutrition during suckling and of post-training ß-endorphin administration on avoidance performances of adult rats

1. The effects of undernutrition during suckling and of post-training ß-endorphin administration on avoidance task were invstigated in adult rats. 2. young rats were undernourished from delivery until weaning (21 days) by feeding their mothers a diet conatining 8% protein (w/w). Mothers of well-nourished rats were fed a 20% protein diet. After weaning, both groups of rats were fed a 20% protein diet until 90-120 days if age, when they were subjected to behavioral sessions. 3. Acquistion was measured in training sessions and retention in test sessions 24 h after training. Beta-endorphin or salina (control) was injected ip immdiately after training. Rats were subjected to shuttle and step-down inhibitory avoidance sessions using footshock of 0.2 or 0.8 mA intensity. 4. Undernutrition during suckling caused hyperreactivity to 0.2 mA footshocks. Beta-endorphin caused amnesia to shuttle avoidance task only in normal rats trained with 0.8 mA. Foor-shocks. In the step-down inhibitory avoidance task, ß-endorphin was amnesic only for normal rats and only for 0.2-mA footshocks. Beta-endorphin was not amnesic in undernourished rats