A preliminary exploration of the potential of Eugenia uvalha Cambess juice intake to counter oxidative stress.

PURPOSE: The ability of foods to aid in the prevention of chronic metabolic diseases, has recently become an area of increased interest. In addition, there is growing interest in exploring the benefits of consuming underutilized fruits as alternatives to commercially available fruits. Eugenia uvalha Cambess (uvaia) is a native fruit of Brazil with great market and phytotherapy potential. The present study was conducted to investigate the effects of uvaia juice (UJ) on the levels of protein carbonyls (PCO) and antioxidant enzymes in the livers of rats fed a high-fat diet. METHODS: Thirty-two female rats were randomly assigned to four groups. The rats were fed either a standard diet (group C) or a high-fat diet (group HF). In addition, groups CUJ and HFUJ were treated with UJ (2mL/day) administered via gavage for 8weeks. RESULTS: In our study, UJ displayed high antioxidant activity (135.14±9.74 GAE/100g). Administration of UJ caused a significantly reduced concentration of rat liver PCO (47.4%), which was associated with a 29% increase in catalase activity. A significant increase in the concentration of oxidized glutathione (GSSG) (15.04±5.08nmol/ml) and a reduction in the reduced glutathione/oxidized glutathione ratio (GSH/GSSG) (11.30±2.68) were found in the HF group, whilst these changes were not observed in the HFUJ group (a result similar to that of group C). CONCLUSIONS: Our results demonstrate that UJ decreases oxidative damage by improving antioxidant efficiency and attenuating oxidative damage to proteins.

Protein-energy malnutrition decreases immune response to Leishmania chagasi vaccine in BALB/c mice.

Protein-energy malnutrition and visceral leishmaniasis are important problems of public health affecting millions of people worldwide. Vaccine efficacy depends on the ability of individuals to mount an appropriate immune response and may be inadequate in malnourished persons. In this study, we used a mouse model to verify the effect of combined protein, iron and zinc deficiency in the response to Leishmania chagasi antigen vaccine. BALB/c mice were fed with a low-protein (3% casein), iron- and zinc-deficient diet or control diet (14% casein and sufficient in zinc and iron). After malnutrition establishment, mice were vaccinated subcutaneously with L. chagasi Ag plus saponin. After vaccination, mice were nutritionally repleted and then all mice were challenged with L. chagasi promastigotes. Four weeks later, liver and spleen parasite load was evaluated. Our data show that vaccine caused a significant reduction in parasite load in spleen and liver from mice fed with control diet. However, splenic parasitism was increased in mice fed with deficient diet and this diet caused a reduction in splenocyte IFN-gamma production in response to the vaccine in repleted mice. These data suggest that malnutrition may alter immune response to L. chagasi vaccine in BALB/c model of infection, even after nutritional repletion.

Baroreflex function in conscious rats submitted to iron overload.

Our hypothesis is that iron accumulated in tissue, rather than in serum, may compromise cardiovascular control. Male Fischer 344 rats weighing 180 to 220 g were divided into 2 groups. In the serum iron overload group (SIO, N = 12), 20 mg elemental iron was injected ip daily for 7 days. In the tissue iron overload group (TIO, N = 19), a smaller amount of elemental iron was injected (10 mg, daily) for 5 days followed by a resting period of 7 days. Reflex heart rate responses were elicited by iv injections of either phenylephrine (0.5 to 5.0 microg/kg) or sodium nitroprusside (1.0 to 10.0 microg/kg). Baroreflex curves were determined and fitted to sigmoidal equations and the baroreflex gain coefficient was evaluated. To evaluate the role of other than a direct effect of iron on tissue, acute treatment with the iron chelator deferoxamine (20 mg/kg, iv) was performed on the TIO group and the baroreflex was re-evaluated. At the end of the experiments, evaluation of iron levels in serum confirmed a pronounced overload for the SIO group (30-fold), in contrast to the TIO group (2-fold). Tissue levels of iron, however, were higher in the TIO group. The SIO protocol did not produce significant alterations in the baroreflex curve response, while the TIO protocol produced a nearly 2-fold increase in baroreflex gain (-4.34 +/- 0.74 and -7.93 +/- 1.08 bpm/mmHg, respectively). The TIO protocol animals treated with deferoxamine returned to sham levels of baroreflex gain (-3.7 +/- 0.3 sham vs -3.6 +/- 0.2 bpm/mmHg) 30 min after the injection. Our results indicate an effect of tissue iron overload on the enhancement of baroreflex sensitivity.

Baroreflex function in conscious rats submitted to iron overload

Our hypothesis is that iron accumulated in tissue, rather than in serum, may compromise cardiovascular control. Male Fischer 344 rats weighing 180 to 220 g were divided into 2 groups. In the serum iron overload group (SIO, N = 12), 20 mg elemental iron was injected ip daily for 7 days. In the tissue iron overload group (TIO, N = 19), a smaller amount of elemental iron was injected (10 mg, daily) for 5 days followed by a resting period of 7 days. Reflex heart rate responses were elicited by iv injections of either phenylephrine (0.5 to 5.0 µg/kg) or sodium nitroprusside (1.0 to 10.0 µg/kg). Baroreflex curves were determined and fitted to sigmoidal equations and the baroreflex gain coefficient was evaluated. To evaluate the role of other than a direct effect of iron on tissue, acute treatment with the iron chelator deferoxamine (20 mg/kg, iv) was performed on the TIO group and the baroreflex was re-evaluated. At the end of the experiments, evaluation of iron levels in serum confirmed a pronounced overload for the SIO group (30-fold), in contrast to the TIO group (2-fold). Tissue levels of iron, however, were higher in the TIO group. The SIO protocol did not produce significant alterations in the baroreflex curve response, while the TIO protocol produced a nearly 2-fold increase in baroreflex gain (-4.34 ± 0.74 and -7.93 ± 1.08 bpm/mmHg, respectively). The TIO protocol animals treated with deferoxamine returned to sham levels of baroreflex gain (-3.7 ± 0.3 sham vs -3.6 ± 0.2 bpm/mmHg) 30 min after the injection. Our results indicate an effect of tissue iron overload on the enhancement of baroreflex sensitivity.

A low protein diet causes an increase in the basal levels and variability of mean arterial pressure and heart rate in Fisher rats.

The correlation between nutrition and cardiovascular related disorders is a well-established fact. Previous work from our Laboratory has suggested a significant compromise of cardiovascular reflexes in conscious rats submitted to a low-protein (LP) diet. Our working hypothesis is that the basal level of mean arterial pressure (MAP), variability of the mean arterial pressure (VMAP), heart rate (HR) and variability of heart rate (VHR) are altered in rats submitted to a protein restricted diet. Two experimental groups were used: control group (normal protein 15%, NP) and malnourished group (low-protein 6%, LP). In order to verify the efficiency of the dietary restriction we measured body weight, total blood protein, plasma albumin, urea and glucose. Our experiments demonstrated that the malnourished rats presented augment levels of basal MAP (LP 122+/-2 mmHg vs. NP 113+/-1 mmHg) and of VMAP (LP 12.8+/-1.5mmHg vs. NP 9+/-1mmHg) when compared to the control group. We observed similar increased levels, in the malnourished group, for both HR (LP 429+/-8 bpm vs. NP 381+/-7bpm) and VHR (LP 67.6+/-8.3bpm vs. NP 44.4+/-4.9bpm). Our results suggest a correlation between the LP diet in Fisher rats and the increased basal levels of mean arterial pressure, HR and their respective variability.

Effects of low-protein diet on the baroreflex and Bezold-Jarisch reflex in conscious rats.

The present study evaluated the effects of a low-protein diet (LP, 6% protein) on cardiovascular reflexes of Male Fisher rats. Three experimental groups, and their respective controls (15% protein), were used: (1) Baroreceptor reflex (BAR); (2) Bezold-Jarisch reflex (BJR); and (3) Prazosin treated. Dietary restriction began after weaning (three weeks) and lasted for a period of five weeks, after which animals were subjected to the experimental protocols. The BAR group was evaluated through injections of phenylephrine (0.5-5.0 microgram/Kg, i.v.) and sodium nitroprusside (0.7-7.0 microgram/Kg, i.v.) while the BJR was evaluated through injections of serotonin (2.5-10 microgram/Kg, i.v.). Our results showed an increased baroreflex gain bradycardia for the LP group (-0.96+/-0.34 vs. -2.12+/-1.06 bpm/mmHg) and a larger bradycardia for the BJR the LP group (160+/-18% greater than controls). Basal cardiovascular parameters were not different between LP and control rats, however LP animals treated with prazosin resulted in a larger fall of blood pressure (-19+/-3 vs. -28+/-5 mmHg). In conclusion, LP rats present an increased responsiveness of BAR and BJR, which could contribute to their normal levels of cardiovascular parameters, in spite of the possible increase in the sympathetic vasomotor tonus observed with the prazosin protocol.

The effect of iron nutritional status on Trypanosoma cruzi infection in germfree and conventional mice.

1. Conventional (CV) and gnotobiotic (GN) female CFW mice were infected with the Y strain of Trypanosoma cruzi. 2. After infection, both CV and GN groups received injections of iron-dextran or desferrioxamine. Non-injected mice served as controls. 3. The parasitemia was more intense in iron-dextran-treated mice. 4. The iron levels in serum, liver, and spleen were: (a) not decreased by desferrioxamine and (b) increased by iron-dextran treatments. 5. An increase in leukocyte numbers was observed in all GN and CV groups after infection. 6. There was no difference in total iron binding capacity (TIBC) and iron saturation transferrin (IST) between GN and CV mice before infection. 7. In CV groups, after infection, TIBC was decreased whereas the levels of IST were increased; in GN the opposite occurred. 8. Trypanosome-specific IgG and IgM antibody levels were raised in the GN group but not in the CV group.

The effect of iron deficiency and iron overload on the evolution of Chagas disease produced by three strains of Trypanosoma cruzi in CFW mice.

1. CFW mice were fed either on control diet or on iron-deficient diet. 2. After 5 months the mice were infected with CL, Y or YuYu strain of Trypanosoma cruzi. 3. On the fifth day after the infection, the mice on control diet were divided in three groups: one group remained as controls, two groups were injected either with desferrioxamine or iron-dextran. 4. The severity of the disease was evaluated by parasitemia and mortality. 5. The experimental groups were compared with the infected group fed on the control diet. 6. In mice fed on the iron-deficient diet, the disease was more severe for CL strain and less severe for Y and YuYu strains. 7. Treatment with desferrioxamine produced a less severe disease with YuYu strain and no difference with the other strains. 8. On Treatment with iron-dextran, the disease became more severe with Y and CL strains; no effect was observed with YuYu strain. 9. These findings may be due to intraspecific differences among the strains.

Neuronal protein biosynthesis by neonatally malnourished and nutritionally recovered rats.

1. The objective of the present study was to examine the reversibility of the effect of neonatal malnutrition on in vivo neuronal protein synthesis. 2. Neonatal malnutrition was achieved by letting the pups suckle mothers fed a low casein diet (6.4%) which decreased the amount of milk produced. The control group was composed of pups from mothers fed a 17% casein diet and kept on the same diet after weaning. A group of pups was undernourished during the suckling period, as above, but fed a 17% casein diet after weaning (recovered group). All animals were killed at 60 days of age. 3. Neuronal cell bodies were separated from forebrain by mechanical disruption of the tissue and centrifugation in a sucrose gradient. 4. Protein biosynthesis was measured by the incorporation of [14C]-leucine into proteins of neuronal cell bodies, after correcting for the specific activity of the precursor. 5. Forebrain cell number and cell size were evaluated by DNA content and the protein/DNA ratio, respectively. 6. The forebrains of the recovered group weighed less than those of the controls, perhaps due to a lower number of cells, which exhibited an average size similar to that of the control group. 7. The rate of protein biosynthesis was similar in malnourished and recovered groups, but both were only 57% of the rate of the control group. 8. We conclude that neonatal malnutrition promotes an irreversible adverse effect on in vivo neuronal protein synthesis by rats.

Neuronal protein biosynthesis by neonatally malnourished and nutritionally recovered rats

1. The objective of the present study was to examine the reversibility of the effect of neonatal malnutritiona on in vivo neuronal protein synthesis. 2. Neonatal malnutrition was achieved by letting the pups suckle mothers fed a low casein diet (6.4%) which decreased the amount of milk produced. The control group was composed of pups from mothers fed a 17% casein diet and kept on the same diet after weaning. A group of pups was undernourished during the suckling period, as above, but fed a 17% casein dietafter weaning (recovered group). All animals were killed at 60 days of age. 3. Neuronal cell bodies were separated from forebraim by mechanical disruption of the tissue and centrifugation in a sucrose gradient. 4. Protein biosynthesis was measured by the incorporation of [14C] - leucine into proteins of neuronal cell bodies, after correcting for the specific activity of the precursor. 5. Forebrain cell number and cell size were evaluated by DNA content and the protein/ DNA ratio, respectively. 6. The forebrains of the recovered group weighed less than those of the controls, perhaps due to a lower number of cells, which exhibited an average size similar to that of the control group. 7. The rate of protein biosynthesis was similar in malnourished and recovered groups, but both were only 57% of the rate of the control group. 8. We conclude that neonatal malnutrition promotes an irreversible adverse effect on in vivo neuronal protein synthesis by rats